Back To Chiropractic CE Seminars Neurology: Hints To Stroke ~ 6 Hours

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Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC By: Larry E. Masula, D.C., DACNB, FAVRB, FAFICC Diplomate American Chiropractic Neurology Board Fellow American Vestibular Rehabilitation Board Fellow Academy of Forensic and Industrial Chiropractic Consultants [email protected]

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, DC, DACNB, FAVRB, FAFICC

Carrick Institute for Advanced Neurological Studies: Frederick C. Carrick, PhD, Cambridge University. Diplomate American Chiropractic Neurology Board Fellow American Vestibular Rehabilitation Board Fellow Academy of Forensic and Industrial Chiropractic Consultants

Evaluation and Management of Dizziness and Balance Disorders, Neil T. Shepard , PhD, director of the Dizziness and Balance Disorders Program at the Mayo Clinic, Rochester, Minnesota, and professor of audiology in the Mayo Clinical School of Medicine. Joel A. Goebel, M.D., FACS. Director, Dizziness and Balance Center Washington University School of Medicine, St. Louis, MO

American Institute of Balance, Continuing Medical Education, Certified in Vestibular Rehabilitation, Ocular Motor Testing, Gaze, Headshake and Positional Testing. Richard E. GANS, PH.D.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Stroke Syndromes Evaluation. This is an introduction to stroke evaluation and how to monitor patients that are suspect for stroke. You will gain a greater understanding of the anatomic Objectives considerations of the various parts of the brain with presentation by the anterior, middle and posterior cerebral arteries, vs. internal capsule strokes, vs. TIA, and brainstem strokes. Pay close attention, it may save you and your patient

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Recommended Reading

 Principles of Neural Science, 4th Edition, Eric R. Kandel, James H. Schwartz, Thomas M. Jessel, McGraw-Hill.

 Technique of the Neurological Examination, 4th Edition, DeMeyer, W. McGraw- Hill.

 Neurological Differential Diagnosis, 2nd Edition, John Patten, Springer 1996.

 Prevention and Management of Comorbidities ©2016 American Heart Association, Inc.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Neuronal Health

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Central Integrative State (Health) of a Neuron Let’s begin by looking at a neuron's environment. There is a constant influx of neuronal membrane potential differences that influence either excitation or inhibition of the neuron. The neuronal environment is constantly changing and strongly influenced by the following. 1. Spatial Summation (multimodal activation) on the receptor. Spatial summation occurs when excitatory potentials from many different pre-synaptic neurons cause the post-synaptic neuron to reach its threshold and fire. 2. The resting state of a neuron may also be influenced by Temporal Summation (high frequency unimodal stimulation) on the receptor. Temporal summation occurs when a single pre-synaptic neuron fires many times in succession, causing the post-synaptic neuron to reach its threshold and fire. 3. The pH of the tissue surrounding the neuron influences the central state of the neuron. 4. Glucose levels being to high or to low may influence the health and resting state of the neuron. In addition, central neurons have a near-exclusive dependence on glucose as an energy substrate, and brain stores of glucose or glycogen are limited. 5. Oxygen tissue saturation is also influential. If circulation ceases, the energy supplies in brain cells are enough to last 3-5 minutes. More about this later. J Clin Invest. 2000 Sep 15; 106(6): 723–731. 6. Temperature changes; heat is excitatory and cold is inhibitory to the neuron. 7. Summation of all presynaptic (+) and (-) input which includes all cortical and segmental integration affects the central integrative state. 8. In summary: stability or fragility of a neuron is based on the FOF of ALL its presynaptic pools or receptor potentials.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC What Drives Nerve Stimulation and The Immediate Early Gene Response? Receptor Activators 5 Messenger System

 Activation from factors on the “5 steps to gene replication” previous slide  1st Messenger System is the  BDNF (brain derived neurotropic Receptor factor)  2nd Messenger System – is a  Neuroendocrine Hormones Carrier Protein within the cytoplasm such as (calmodulin) which  Neurotransmitters stimulates the…  Good Cytokines  3rd Messenger System, a Protein  A Non-inflamed environment Kinase

 4th Messenger System causes a Phosphoprotein to activate the nucleus Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC  5th is a Nuclear Transcribed Protein Understanding Neurons – the Big Picture

 Sufficient stimulation of receptors to bring the neuron to threshold results in activation of the 1st order afferent (sensory) neuron.

 Activation of the 2nd order afferent neurons is dependent on the FOF of its pre-synaptic neuronal pool (1st order neurons).

 Activation of the thalamus and eventually all cortical structures is dependent upon the normal frequency of firing (FOF) of ALL pre- synaptic neuronal pools of the somatosensory system).

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC When the nucleus gets activated via the 5- messenger system, it makes raw proteins. These proteins are further modified in the endoplasmic reticulum and placed in a secretory granule which are then transported down microtubules to a synaptic vesicle where they are stored at the axon terminal. Once released into the synapse excess neurotransmitter substance is brought back into the cell via a retrograde vesicle where it is broken down and re-used, recycled and re-manufactured. The Post synaptic response is a thankyou!

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC What maintains health of the neuron?

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC 1. Fuel Glucose O2 2. Activation

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Cell Death Over the last 15 years, evidence has emerged indicating that energetics considerations and energy substrate limitations are not solely responsible for the brain’s heightened vulnerability to ischemia. Rather, it appears that the brain’s intrinsic cell-cell and intracellular signaling mechanisms, normally responsible for information processing, become harmful under ischemic conditions, hastening energy failure and enhancing the final pathways underlying ischemic cell death in all tissues, including free radical production, activation of catabolic enzymes, membrane failure, apoptosis, and inflammation

Inflammation/trauma/ischemia lead to free radical formation generated in the mitochondria. These conditions also activate microglial cells as do macrophages that enter from the periphery. Macrophage “posers” evolve into bad cytokines that trigger the NMDA receptors on the surface of the neuronal membrane at different rates causing the Central Integrative State of the neuron to shift. This results in excessive Ca+ influx resulting in one cell to do something different from the others = a bad orchestra.

Larry E. Masula, D.C., DACNB, FAVRB, FAFICC, FAFICC Neuronal Cell Death

 Pro-inflammatory cytokines are released which further damage the oligodendrocytes and other astrocytes. The blood brain barrier breaks down triggering a TH-1 and TH-17 response causing even more massive inflammation. The bi-lipid membrane becomes damaged and neuronal microtubules breakdown, which further primes the Glial system → more TND and a domino effect occurs.

 Glial cells, sometimes called neuroglia or simply glia are non-neuronal cells that maintain homeostasis. They hold neurons in place, supply O2 and nutrition to neurons, insulate one neuron from another, destroy pathogens and remove dead neurons. When affected they can release inflammatory “BAD” cytokines which perpetuate the above.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC  Is altered by the frequency of firing (FOF) of all presynaptic pool input into the neuron (Activation)

 Therefore, it is extremely important to identify and manage improper Fuel in the form of Dysglycemia, Hypoglycemia, Brief summary: Metabolic Syndrome, Insulin resistance. (Fuel - glucose)

Cellular  Identify and manage anemia (Fuel – Survival O2)  Assure an adequate protein and fat intake

 Identify and manage Inflammatory conditions, Infections and Autoimmunity

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC  Do you know how to evaluate for stroke, what clinical things to look for and rapidly move The Big Picture through differentials as it pertains to cortical and capsular strokes.

Concept  Do you know where you fit as it pertains to the treatment of stroke?

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC What is a Stroke?

A stroke is a “brain attack”. It can happen to anyone at any time. It occurs when blood flow to an area of brain is cut off. When this happens, brain cells are deprived of oxygen and begin to die within 1-2 minutes. When brain cells die during a stroke, abilities controlled by that area of the brain such as memory and muscle control are lost. Stroke (or Cerebrovascular accident) is a syndrome of rapidly developing clinical signs of focal or global disturbance of cerebral function, with symptoms lasting 24 hours or longer or leading to death with no apparent cause other of vascular origin.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC What is a Stroke?

How a person is affected by their stroke depends on where the stroke occurs in the brain and how much the brain is damaged. For example, someone who had a small stroke may only have minor problems such as temporary weakness of an arm or leg. People who have larger strokes may be permanently paralyzed on one side of their body or lose their ability to speak. Some people recover completely from strokes, but more than 2/3 of survivors will have some type of disability. Those over 65 have the greatest stroke probability.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC What is a Stroke? “Types of stroke”

 Hemorrhagic Stroke - A brain aneurysm burst or a weakened blood vessel leak (hemorrhagic) is one of two types of stroke. While the least common of the two types of stroke it most often results in death.

 Ischemic Stroke - A blood vessel carrying blood to the brain is blocked by a blood clot (ischemic) is one type of stroke.

 What Is TIA? - When blood flow to part of the brain stops for a short period of time, also called transient ischemic attack (TIA), it can mimic stroke-like symptoms. These appear and last less than 24 hours before disappearing.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Transient Ischemic Attack (TIA)

 A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by loss of blood flow (ischemia) in the brain, spinal cord, or retina, without tissue death (infarction). ... TIA causes the same symptoms associated with stroke, such as weakness or numbness on one side of the body. Numbness or weakness generally occur on the opposite side of the body from the affected hemisphere of the brain. A TIA may cause sudden dimming or loss of vision, difficulty speaking or understanding language, slurred speech, and confusion.  TIA and ischemic stroke share a common cause. Both result from a disruption in blood flow to the central nervous system. In ischemic stroke, symptoms generally persist beyond 7 days. In TIA, symptoms typically resolve within 1 hour.  The occurrence of a TIA is a risk factor for eventually having a stroke. 5-10 percent of patients presenting with TIA will have a stroke within the following week. Recognition that a TIA has occurred is an opportunity to start treatment.

 1. Lovett JK, Dennis MS, Sandercock PA, Bamford J, Warlow CP, Rothwell PM. Very early risk of stroke after a first transient ischemic attack. Stroke. 2003;34:e138–40.

 2. Johnston SC, Gress DR, Browner WS, Sidney S. Short-term prognosis after emergency department diagnosis of TIA. JAMA. 2000;284:2901– 6.

 3. Rothwell PM, Giles MF, Flossmann E, Lovelock CE, Redgrave JN, Warlow CP, et al. A simple score (ABCD) to identify individuals at high early risk of stroke after transient ischaemic attack. Lancet. 2005;366:29–36.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC TIA

 The ABCD (Age, Blood pressure, Clinical features, Duration of symptoms) rule for predicting stroke risk after TIA was developed using data from patients with possible TIA who were referred to a neurologist by their primary care physician from 1981 to 1986 and who, on further evaluation, were suspected to have a probable or definite TIA. The ABCD rule was validated in a separate group of patients from the Oxford Vascular Study who were referred from 2002 to 2004.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Applying the Evidence

 A 52-year-old patient who is hypertensive presents to your office after an episode of transient weakness in his right arm that occurred several days ago. The episode lasted about five minutes and was not accompanied by speech difficulty. His blood pressure has been well controlled and measures 130/78 mm Hg during the office visit. You diagnose him with possible TIA. What is his risk of stroke within the next seven days?  Answer: Using the ABCD clinical prediction rule, you give the patient two points for unilateral weakness and zero points for age, blood pressure, and duration of symptoms. Therefore, you conclude that the patient has low risk of stroke (none of 184 patients with possible TIA and none of 62 with probable or definite TIA who had a score of three or lower had a stroke within seven days), and you and the patient decide that outpatient evaluation is appropriate. About 10% of patients will have a stroke in the first week, and about 5% each year thereafter.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC  Ischemic 80%  Thrombotic 60%  Embolic 20% Stroke Statistics  Hemorrhagic 20%  Intracerebral hemorrhage 12%  Subarachnoid hemorrhage 8%

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Stroke Statistics  Stroke kills about 140,000 Americans each year—that’s 1 out of every 20 deaths.1  Someone in the United States has a stroke every 40 seconds. Every 4 minutes, someone dies of stroke.2  Every year, more than 795,000 people in the United States have a stroke. About 610,000 of these are first or new strokes.2  About 185,000 strokes—nearly 1 of 4—are in people who have had a previous stroke.2  About 87% of all strokes are ischemic strokes, in which blood flow to the brain is blocked.2  Stroke costs the United States an estimated $34 billion each year.2 This total includes the cost of health care services, medicines to treat stroke, and missed days of work.  Stroke is a leading cause of serious long-term disability.2 Stroke reduces mobility in more than half of stroke survivors age 65 and over

 1. Vital Signs: Recent trends in stroke death rates – United States, 2000-2015. MMWR 2017;66.

 2. Benjamin EJ, Blaha MJ, Chiuve SE, et al. on behalf of the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics—2017 update: a report from the American Heart Association. Circulation. 2017;135:e229-e445.  While approximately two-thirds of strokes happen in people over age 65, people under age 65 can still have a stroke. Stroke risk does increase with age, but anyone at any age can have a stroke.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Stroke Statistics

 According to a review article published in The Medical Clinics of North America, “most patients survive a first-time ischemic stroke but are at high risk for recurrent stroke as well as concomitant cardio- and peripheral vascular diseases. Patients are at highest risk of stroke in the first few days after TIA; therefore, rapid evaluation of stroke risk is of utmost importance.”

 For complete information, see:

 Caprio FZ, Sorond FA. Cerebrovascular disease: primary and secondary stroke prevention. Med Clin North Am. 2019;103(2):295-308.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Stroke Statistics

 Amongst ischemic strokes, cardio embolism, large vessel atherosclerosis, and small vessel disease account for 65% of cases; the remaining are due to other definite causes, and are considered cryptogenic,” according to information cited in a review article published in The Medical Clinics of North America. Cryptogenic stroke (CS) is defined as cerebral ischemia of obscure or unknown origin. The cause of CS remains undetermined because the event is transitory or reversible, investigations did not look for all possible causes, or because some causes truly remain unknown. One third of the ischemic strokes are cryptogenic.

 For complete information, see:

 Caprio FZ, Sorond FA. Cerebrovascular disease: primary and secondary stroke prevention. Med Clin North Am. 2019;103(2):295-308.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Stroke Statistics: Ischemic stroke and transient ischemic attack

 “AF accounts for 10% to 12% of all ischemic strokes and is typically detected on electrocardiograms or telemetry or on subsequent prolonged rhythm monitoring after stroke,” according to information cited in a review article published in The Medical Clinics of North America.

 For complete information, see:

 Caprio FZ, Sorond FA. Cerebrovascular disease: primary and secondary stroke prevention. Med Clin North Am. 2019;103(2):295-308.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Ischemic stroke and transient ischemic attack

 According to a review article published in The Medical Clinics of North America, “timely treatment of acute ischemic stroke with systemic thrombolysis and mechanical thrombectomy leads to improved functional outcomes.” Moreover, according to information cited in the same, “in the acute setting of an ischemic stroke, timely treatment, even small reductions on the order of minutes, leads to significant increase in disability free life.”

 For complete information, see:

 Caprio FZ, Sorond FA. Cerebrovascular disease: primary and secondary stroke prevention. Med Clin North Am. 2019;103(2):295-308.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC  Atrial Fibrillation 17 times

Stroke  Hypertension 2-4 Statistics: times  Cardiac Disease 2-4 times

 No Exercise 1.8-3.5 Risk Factors: times Estimated  Diabetes 1.5-25. times

Increase in  Smoking 1.5-2.5 Risk times  Heavy Alcohol Use 1-3 times

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Stroke Warning Signs

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Thrombotic strokes – occur during sleep when the Helpful circulation is least active bedside and Hemorrhage and Embolism – clinical data during activity when circulation is active

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC 1. Past, personal and family history (presence of diabetes, coronary heart disease, hypertension, pt. on anticoagulants) 2. History of old strokes or TIA’s Helpful 3. Time of onset of symptoms bedside and 4. Activity at the time of onset of clinical data symptoms 5. Temporal course and progression 6. Accompanying symptoms – headache, vomiting, decreased consciousness Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Viability of brain tissue is Window of preserved if perfusion is Opportunity restored within a critical time period ( 2-4 hours)

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Nothing Replaces a Good Bedside Neurological Examination

Bedside Diagnostic mnemonic “Gem” V – Vascular I _ Infectious N – Neoplastic, Neurological D – Degenerative I – Inflammatory C – Connective tissue/muscle A – Autoimmune T – Trauma E – Endocrine/environmental S - Soft tissue

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC VASCULAR: Cardiovascular Disease and Cerebrovascular Disease

 Everything Condition is Considered Vascular Until Proven Otherwise  Arrhythmias  Tachycardia  Bradycardia  Ischemic cardiomyopathy  Vasovagal syncope  Carotid sinus hypersensitivity  Conduction blocks w/ elongation of the PR interval  Brain ischemia  Etc.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Facial drooping: one side of the face does not move as well as the other side (forehead, The FAST eyes, mouth). mnemonic for Arm weakness: unilateral weakness or recognizing positive pronator drift sign.

Anterior Speech difficulty: slurring of speech, wrong Circulation words or inability to speak based strokes: Time: a patient with any of the above should be sent to the hospital immediately

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Diplopia (or other visual problems) Mnemonic for Signs and Dysphagia Symptoms of (posterior Drop attacks (sudden weakness in face/arm/ leg circulation) Dizziness (vertigo, light-headedness, giddiness) Vertebrobasilar Dysphagia

Ischemia Ataxia of gait (hemiparesis)

“5 D’s And 3 N’s” Nausea (possibly with vomiting) Numbness (hemianesthesia)

Nystagmus

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Vascular Anatomy

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Blood Supply to the Anterior Brain

The brain receives blood from the Internal Carotid Arteries, which arise at the point in the neck where the common carotid arteries bifurcate. The internal carotid arteries branch to form two major cerebral arteries, the anterior and middle cerebral arteries

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Blood Supply to the Posterior Brain The right and left vertebral arteries come together at the level of the pons on the ventral surface of the brainstem to form the midline basilar artery. The basilar artery joins the blood supply from the internal carotids in an arterial ring at the base of the brain (in the vicinity of the hypothalamus and cerebral peduncles) called the circle of Willis. The posterior cerebral arteries arise at this confluence, as do two small bridging arteries, the anterior and posterior communicating arteries. Conjoining the two major sources of cerebral vascular supply via the circle of Willis presumably improves the chances of any region of the brain continuing to receive blood if one of the major arteries becomes occluded

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Brainstem Vasculature The Circle of Willis The vertebral arteries enter the cranium through the foramen magnum of the occipital bone. Branches off the left and right vertebral arteries merge into the anterior spinal artery supplying the anterior aspect of the spinal cord, found along the anterior median fissure. The two vertebral arteries then merge into the basilar artery, which gives rise to branches to the brain stem and cerebellum. The left and right internal carotid arteries and branches of the basilar artery all become the circle of Willis, a confluence of arteries that can maintain perfusion of the brain even if narrowing or a blockage limits flow through one part .

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Anterior Spinal Artery

The anterior spinal artery arises bilaterally as two small branches near the termination of the vertebral arteries. One of these vessels is usually larger than the other, but occasionally they are about equal in size. Descending in front of the medulla oblongata, they unite at the level of the foramen magnum. The single trunk descends in the front of the medulla spinalis, extending to the lowest part of the medulla spinalis. It is continued as a slender twig on the filum terminale.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Internal Carotid Artery

The carotid arteries are major blood vessels in the neck that supply blood to the brain, neck, and face. There are two carotid arteries, one on the right and one on the left. In the neck, each carotid artery branches into two divisions: The internal carotid artery supplies blood to the brain. The internal carotid then divides to form the anterior cerebral artery and middle cerebral artery. The internal carotid artery can receive blood flow via an important collateral pathway supplying the brain, the cerebral arterial circle, which is more commonly known as the Circle of Willis. Importantly, for patients with stroke or TIA attributed to severe (> 70%) extracranial internal carotid artery (ICA) stenosis.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC The internal capsule is described as having a:  Anterior Limb  Genu  Posterior Limb

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Aneurysms and potential stroke sites in the Circle of Willis

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC What Type of Stroke is it?

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Vascular Territories

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Internal Carotid Artery A 68-year-old white man with a history of hypercholesterolemia and 50-pack-year smoking presented with transient episodes affecting the right side of his body. During the first episode, he had weakness of his right leg, lasting for about 10 minutes. The second spell happened 1 week later and was characterized by speech difficulties, right facial drop, and right arm weakness that lasted for 2 hours. Brain magnetic resonance imaging (MRI) with diffusion- weighted imaging demonstrated two small strokes in the left frontal lobe, one in the ACA territory and the second one in the MCA distribution. Magnetic resonance angiography (MRA) of the head and neck was remarkable for a 70–80% stenosis of the left ICA, confirmed by carotid ultrasound.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Internal Carotid Artery  Main trunk occlusions may be indistinguishable from MCA occlusions, ACA occlusions, or occlusion of both. It also may be completely asymptomatic given the variability of anastomosis.

 What distinguishes ICA occlusions from others is the presence of ipsilateral Amaurosis Fugax (sudden onset blindness) caused by occlusion of the ophthalmic artery. A carotid pulse may be absent, the patient may also have a Horner’s syndrome.  Anterior Choroidal Artery is the last branch to originate from Internal Carotid Artery. It supplies the optic tract, posterior limb of internal capsule, branches to midbrain, and lateral geniculate nucleus of the thalamus. An Anterior Choroidal Artery Occlusion is a rare entity characterized by the triad of contralateral hemiplegia and hemianesthesia, and contralateral hemianopias.  Extracranial internal carotid artery stenosis was associated with 8.0% of all ischemic strokes

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Hollenhorst Plaques

 Hollenhorst first described cholesterol plaques int the retinal arterioles in 1958  Formed from cholesterol deposition, most commonly originating from the ipsilateral carotid artery  Patients are largely asymptomatic due to the malleability of the plaque and persistent vascular perfusion and around the emboli.  This may be an incidental finding during fundoscopy  Frequently, the plaques dislodge and may not be noted on subsequent examinations. Determine if symptomatic for: ◦ Sudden dizziness, visual disturbances, slurred speech, hemiparesis, or Hx of CVA

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Ocular Ischemic Syndrome

 Widespread ischemia to the eye may result when the carotid artery is occluded at least 90%.  Symptoms:  Decreased vision  Peri-orbital eye pain  Headache  Amaurosis fugax  Extended visual recovery after photo stress.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Carotid Auscultation

 Using Bell Mode

 For low-frequency sounds

 Heart Murmur/Carotid Bruit

 Rest the bell lightly on the patient. When the diaphragm membrane is suspended, the membrane resonates low-frequency sounds.

 Using Diaphragm Mode

 For high-frequency sounds

 Lungs/Normal Heart

 Use firm pressure on the head. This blocks low-frequency sounds and allows you to hear higher frequency sounds.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Hollenhorst Work-Up

 Lipid Panel  Carotid Auscultation  Carotid Duplex Consider duplex imaging for patients over the age of 60 with comorbid systemic vascular conditions and evidence of pertinent retinal findings.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Computed Tomography Angiography

 Performed to accurately determine the degree of carotid stenosis prior to surgical intervention.

 The procedure uses an intravenous contrast which allows for clear imaging of the arterial lumen

 CTA has a sensitivity of 85% and specificity of 93% when performed on patients with stenosis percentages between 70% and 99%.12

 CTA is especially beneficial when duplex results are suggestive of total occlusion, as there may be mild patency of the artery allowing for surgical intervention.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Carotid Stent

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC A 60-year-old male with a history of diabetes and hypertension presents with weakness, dizziness and abnormal speech for the past 24 hours. The patient’s spouse states that he recently started acting “funny,” and his symptoms have been worsening. Upon examination, the patient appears confused but is able to follow your commands. During the cardiac examination, a left carotid bruit is auscultated. During the neurological examination, a sensory and motor loss is noted in the right lower leg. The patient’s speech sounds halting and effortful, but he is able to repeat words back to you. The patient does not have evidence of cranial nerve abnormalities on exam. What syndrome describes the ischemic stroke this patient suffers from?

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Anterior Cerebral Artery

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Anterior Cerebral Artery The anterior cerebral artery is the smaller of the two terminal branches. It commences at the medial aspect of the Sylvian fissure passing anterior and medial to the optic nerve and is closely related to the anterior cerebral artery of the opposite side and is joined to it by the small anterior communicating artery. The anterior cerebral artery has cortical and central branches which will be dealt with below. The recurrent artery of Heubner also arises from the anterior cerebral artery. This branch supplies the internal capsules anterior limb, caudate nucleus, and putamen. Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Anterior Cerebral Artery

The anterior cerebral artery (ACA) arises below the anterior perforated substance and runs anteromedially to the interhemispheric fissure, where it joins the opposite ACA by way of the anterior communicating artery (ACoA). The ACA supplies the medial surface of the cerebrum and the upper border of the frontal and parietal lobes largely affecting the midline frontal and motor cortex projections. One of the first branches of the ACA is the recurrent branch of Huebner aka medial striate artery, Its vascular territory is the basal ganglia (anteromedial section of the caudate nucleus, parts of the putamen and septal nuclei and the anterior inferior section of the internal capsule.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Motor cortex homunculus Remember the ACA distribution is midline

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Anterior Cerebral Artery

 The ACA is often divided into A1  The anterior cerebral vasculature and A2 segments. The A1 segment gives off mainly branches that are is the horizontal, proximal portion MEDIAL in nature and do not that extends from the origin of the venture laterally as much. As the ACA to its union with the ACA moves anterior from proximal contralateral ACA by way of the to distal it gives off: ACoA. The A2 segment is the  Huebner’s branch (first branch) portion of the ACA that is distal to the ACoA. It runs superiorly into the  Medio-frontal orbital branch (midline) interhemispheric fissure,  Frontal polar branch coursing around the genu of the corpus callosum.  Callosomarginal branch and pericallosal split. The Callosomarginal gives 3 collaterals; the anterior, middle and posterior frontal branches.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Anterior Cerebral Artery Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC ACA

Strokes or occlusions in this vessel’s pathway does occur. Main branch or proximal main trunk occlusion is rare but does occur. There are atypical and typical findings.

The first branch is the recurrent branch of Huebner which supplies parts of the internal capsule and basal ganglia. In particular the portion of the capsule that houses the descending motor fibers (corticobulbar) to the cranial nerves and contralateral arm.

A block prior to the recurrent branch of Huebner you will have a different scenario due to injury to the anterior limb of the internal capsule manifested as upper motor neuron (lower face) facial weakness, a spastic arm not flaccid, a contralateral hemiplegic leg due to the cortical loss and sensory loss of the affected leg (remember where the leg resides on the homunculus). If the recurrent artery of Huebner is spared, then atypical findings will be flaccid paralysis of the leg which later becomes spastic and cortical sensory loss to the leg. At this point there will likely be NO involvement of the face and the arm. Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC ACA

 The legs are represented in the midline in both the motor and sensory strips. This region as previously discussed is vascularized by the Anterior Cerebral Artery. Each artery supplying its own side. The cause of a patient presenting with bilateral lower extremity upper motor neuron findings most likely would not be vascular and a midline tumor would be suspect.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC ACA Imaging

 The crucial step in the evaluation of stroke patients is to obtain brain imaging to ascertain the type and characteristics of the stroke. In this regard, non-contrast CT of the head is the imaging modality of choice. Ischemic changes may classify as acute, subacute, and chronic, depending on the time in which they present after the onset of stroke. CT scan can also rule out intracranial hemorrhage  As in strokes involving other areas of the brain, magnetic resonance imaging is also of critical value in the diagnosis of ACA strokes. MRI with diffusion-weight imaging is a highly useful modality, which facilitates the demarcation of ischemic boundaries in the territory of the ACA. MR angiography can be a helpful adjunct in the evaluation of stroke mechanisms. The goal of completing head CT or MRI should be 25 min or less within patient arrival.  The National Institutes of Neurological Disorders and Stroke (NINDS) established time frame goals in the evaluation of stroke patients in the ED: door to physician less than 10 min, door to stroke team less than 15 min, door to CT scan less than 25 min, door to drug less than 60 min  In other words, GET THEM TO THE HOSPITAL FAST!

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Anterior Cerebral Artery Infarction A 64-year-old man developed right lower extremity weakness.

Anterior Cerebral Artery Infarction. Diffusion-weighted MRI scans. Note the high signal intensity in the distribution of the left anterior cerebral artery. As the anterior cerebral artery supplies the medial frontal lobe, an infarct in this distribution predominantly results in weakness of the contralateral leg.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Middle Cerebral Artery

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Middle Cerebral Artery Gross Anatomy

The middle cerebral artery (MCA) is one of the three major paired arteries that supply blood to the brain. The MCA arises from the internal carotid artery as the larger of the two main terminal branches (the other being the anterior cerebral artery), coursing laterally into the lateral sulcus where it branches to perfuse the cerebral cortex.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC MCA

 M1Segments

 medial lenticulostriate penetrating arteries

 lateral lenticulostriate penetrating arteries

 anterior temporal artery

 polar temporal artery

 uncal artery (which may branch from the anterior choroidal artery)

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Middle Cerebral Artery

Superior terminal branch  Lateral Orbitofrontal artery  Prefrontal artery  Precentral (pre-Rolandic)  Central (Rolandic)  Postcentral (anterior parietal) Inferior terminal branch  Anterior temporal artery  Middle temporal artery  Temporooccipital artery  Posterior parietal  Angular re-Rolandic (precentral) and Rolandic (central) sulcal arteries

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Middle Cerebral Artery

 The middle cerebral artery territory is the most commonly affected territory in a cerebral infarction, due to the size of the territory and the direct flow from internal carotid artery into the middle cerebral artery, providing the easiest path for thromboembolism.  Clinical presentation  The neurological deficit will depend on the extent of the infarct and hemispheric dominance, and include:  contralateral hemiparesis  contralateral hemisensory loss  hemianopia  aphasia: if the dominant hemisphere is involved; may be expressive in anterior MCA territory infarction, receptive in posterior MCA stroke, or global with extensive infarction  neglect: entire hemi-neglect of the non-dominant hemisphere (most often the entire left side due to a right brain lesion. (May result in Alien Hand Syndrome )

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Middle Cerebral Artery

Terminal Branch Occlusion (4 major branches) Branch Dominant Side Nondominant side Precentral Broca’s aphasia, flaccid Flaccid monoplegia of facial and arm paralysis arm and face Central Facial and arm weakness Flaccid monoplegia of rm with mild expressive and face aphasia Post. Parietal Complete aphasia, Cortical sensory loss of possible hemiparesis and arm and face and sensory loss apraxia's Superior Temporal Wernicke’s area Cortical sensory loss of arm and face and apraxia's

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Definitions

 Left MCA stroke may include Broca’s Aphasia. Expressive aphasia, also known as Broca's aphasia, is a type of aphasia characterized by partial loss of the ability to produce language (spoken, manual, or written), although comprehension generally remains intact. Speech is effortful and it is hard to convey thoughts through writing. The client knows what they want to say but cannot find the words.  Receptive (Wernicke’s) Aphasia: fluent. The client speaks fluently, but the words often do not make sense. It is hard to process (receive) spoken or written words as well. Patients with Wernicke's aphasia have impaired comprehension of their speech and thus do not recognize the errors that they are making. As a result of the occlusion in the left middle cerebral artery.  Complete Aphasia. In this form of aphasia the ability to grasp the meaning of spoken words is chiefly impaired, while the ease of producing connected speech is not much affected. Therefore Wernicke's aphasia is referred to as a 'fluent aphasia.'

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC MCA Strokes

Definition of topographic patterns using diffusion weighted magnetic resonance imaging. Territorial infarcts (A) showing involvement of more than one M2 branch of the middle cerebral artery (MCA), or MCA stem involvement and cortical infarcts (B), showing involvement of only one M2 branch of the MCA. Subcortical infarcts (C) are subdivided into deep perforator (DP) infarcts, border zone infarcts including either internal (IB) or external border zone (EB) infarcts, and superficial perforator (SP) infarcts.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Middle Cerebral Artery Strokes

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Posterior Cerebral Artery

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Posterior Cerebral Artery

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Posterior Cerebral Artery

The basilar artery gives off paramedian branches that supply the oculomotor (III) nerve nucleus and red nucleus (RN). • A larger branch, the posterior cerebral artery, courses laterally around the midbrain, giving off a basal branch that supplies the cerebral peduncle (CP) and a dorsolateral branch supplying the spinothalamic tract (ST) and medial lemniscus (ML). • The posterior cerebral artery continues (upper arrows) to supply the thalamus, occipital lobe, and medial temporal lobe

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC PCA vascular territory

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Posterior Cerebral Artery PCA stroke assessment for the practicing chiropractor is important primarily due to the nature of the presenting symptoms of headaches, lightheadedness, difficulty focusing and neck pain which are often seen in the chiropractic office. The posterior cerebral artery (PCA) is one of a pair of blood vessels that supply oxygenated blood to the posterior aspect of the brain (occipital lobe) in human anatomy. It arises near the intersection of the posterior communicating artery and the basilar artery and connects with the ipsilateral middle cerebral artery (MCA) and internal carotid artery via the posterior communicating artery (PCommA).

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Posterior Cerebral Artery

 Central branches  Also known as the perforating branches:  Thalamoperforating and thalamogeniculate or postero-medial ganglionic branches: a group of small arteries which arise at the commencement of the posterior cerebral artery: these, with similar branches from the posterior communicating, pierce the posterior perforated substance, and supply the medial surfaces of the thalami and the walls of the third ventricle.  Peduncular perforating or postero-lateral ganglionic branches: small arteries which arise from the posterior cerebral artery after it has turned around the cerebral peduncle; they supply a considerable portion of the thalamus.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Posterior Cerebral Artery

 Cortical branches  The cortical branches are:  Anterior temporal, distributed to the uncus and the anterior part of the fusiform gyrus  Posterior temporal, to the fusiform and the inferior temporal gyri

 Lateral occipital, which branches into the anterior, middle and posterior inferior temporal arteries  Medial occipital, which branches into the:

 Calcarine, to the cuneus and gyrus lingualis and the back part of the convex surface of the occipital lobe

 Parieto-occipital, to the cuneus and the precuneus  Splenial, or the posterior pericallosal branch, sometimes anastomoses with the anterior cerebral artery (ACA), and may not be present if the ACA wraps around the corpus callosum

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Posterior Cerebral Artery

 Structures involved

 Peripheral territory (Cortical branches)

 Homonymous hemianopia (often upper quadratic): Calcarine cortex or optic radiation nearby.

 Bilateral homonymous hemianopia, cortical blindness, awareness or denial of blindness; tactile naming, achromatopia (color blindness), failure to see to-and-fro movements, inability to perceive objects not centrally located, apraxia of ocular movements, inability to count or enumerate objects, tendency to run into things that the patient sees and tries to avoid: Bilateral occipital lobe with possibly the parietal lobe involved.

 Verbal dyslexia without agraphia, color anomia: Dominant calcarine lesion and posterior part of corpus callosum.

 Memory defect: Hippocampal lesion bilaterally or on the dominant side only.

 Topographic disorientation and prosopagnosia: Usually with lesions of nondominant, calcarine, and lingual gyrus.

 Simultanagnosia, hemi-visual neglect: Dominant visual cortex, contralateral hemisphere.

 Unformed visual hallucinations, peduncular hallucinosis, metamorphopsia, teleopsia, illusory visual spread, palinopsia, distortion of outlines, central photophobia: Calcarine cortex.

 Complex hallucinations: Usually nondominant hemisphere.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Posterior Cerebral Artery

 Choroidal branches

 See also: Anterior choroidal artery

 Medial posterior choroidal branches: run forward beneath the splenium of the corpus callosum and supply the tela choroidea of the third ventricle and the choroid plexus.

 Lateral posterior choroidal branches: small branches to the cerebral peduncle, fornix, thalamus, and the caudate nucleus.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Posterior Cerebral Artery

 Central territory (Ganglionic branches)  Thalamic syndrome: sensory loss (all modalities), spontaneous pain and dysesthesias, choreoathetosis, intention tremor, spasms of hand, mild hemiparesis, contralateral hemianesthesia: Posteroventral nucleus of thalamus; involvement of the adjacent subthalamus body or its afferent tracts.  Thalamoperforate syndrome: crossed cerebellar ataxia with ipsilateral third nerve palsy (Claude's syndrome): Dentatothalamic tract and issuing third nerve.  Weber's syndrome: third nerve palsy and contralateral hemiplegia: Third nerve and cerebral peduncle.  Contralateral hemiplegia: Cerebral peduncle.  Paralysis or paresis of vertical eye movement, skew deviation, sluggish pupillary responses to light, slight miosis and ptosis (retraction nystagmus and "tucking" of the eyelids may be associated): Supranuclear fibers to third nerve, interstitial nucleus of Cajal, nucleus of Darkschewitsch, and posterior commissure.  Contralateral rhythmic, ataxic action tremor; rhythmic postural or "holding" tremor (rubro-tremor)

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Posterior Cerebral Artery

 Clinical relevance

 Stroke

 Contralateral loss of pain and temperature sensations.

 Visual field defects (contralateral hemianopia with macular sparing).

 Prosopagnosia with bilateral obstruction of the lingual and fusiform gyri.

 Superior Alternating Syndrome (Weber's syndrome)

 Contralateral deficits of facial nerve (only lower face, upper face receives bilateral input), vagus nerve and hypoglossal nerve

 Ipsilateral deficit of oculomotor nerve

 Horner's Syndrome

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Weber Syndrome

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Right Homonymous Hemianopia (PCA stroke)

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC  The internal capsule, a white matter structure, is a unique location where a large number of motor and sensory fibers travel to and from the cortex. Damage of any kind in this location will cause some relatively unique findings that can Internal Capsule: allow you to localize the lesions to the internal capsule by exam alone. Introduction to  Location the Exam for  The internal capsule is one of the subcortical structures of the brain. Internal Capsular  Subcortical structures: internal capsule, caudate, putamen, Globus pallidus, thalamus, brainstem Stroke  The anterior limb of the internal capsule separates the caudate nucleus and lenticular nucleus  The posterior limb separates the thalamus and lenticular nucleus

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Internal Capsule Types of fibers

 Anterior limb: frontopontine fibers (frontal cortex to pons), thalamocortical fibers (thalamus to frontal lobe)

 Genu (angle): corticobulbar fibers (cortex to brainstem)

 Posterior limb: corticospinal fibers (cortex to spine), sensory fibers

 Blood Supply

 Anterior limb: mainly fed by the lenticulostriate branches of middle cerebral artery(MCA), less often branches of anterior cerebral artery (ACA)

 The lenticulostriate arteries are small penetrating blood vessels that supply blood flow to most of the subcortical structures.

 Genu: lenticulostriate branches of MCA

 Posterior limb: lenticulostriate branches of MCA & anterior choroidal artery (AChA) of internal carotid artery Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Symptoms and Signs Clinical Weakness of the face, arm, and/or leg (pure motor stroke)

Findings in • Known as one of the classic types of lacunar infarcts, a pure motor stroke is the result of an infarct in the internal capsule. Pure motor stroke caused by an infarct in the internal capsule is the most Internal common lacunar syndrome. Upper motor neuron signs: hyperreflexia, Babinski sign, Capsular Hoffman present, clonus, spasticity

Stroke Mixed sensorimotor stroke

• Since both motor and sensory fibers are carried in the internal capsule, a stroke to the posterior limb of the internal capsule (where motor fibers for the arm, trunk and legs and sensory fibers are located) can lead to contralateral weakness and contralateral sensory loss

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Anterior Choroidal Artery branch of the Carotid artery, Infarct of Internal Capsule

 Clinical Signs:

 Contralateral Hemianopia

 Possible contralateral hemiplegia or hemiparesis

 Transient anterograde amnesia

 Transient emotional instability

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Lenticulostriate artery branch of MCA Internal Capsule Stroke

 Lenticulostriate infarcts result from ischemia within the territory supplied by the deep perforating branches of the middle cerebral artery (MCA). They are too often associated with infarctions of the deep perforating branches of the internal carotid artery.  Clinical signs include contralateral motor deficit and or sensory loss of the face and body. The principal mechanism for lenticulostriate infarction seems to be an embolism of cardiac origin.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Huebner’s Branch of ACA

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Huebner’s Branch of ACA Internal Capsule Stroke

Recurrent artery of Heubner, also known as the medial striate artery or long central artery, is the largest perforating branch from the proximal anterior cerebral artery (ACA) and is the only one routinely seen on angiography. It is named after Johann Otto Leonhard Heubner, a German pediatrician (1843-1926), who first described his eponymous vessel in 1872.

 Clinical manifestations of occlusion:

 unilateral

 weakness contralateral arm

 weakness contralateral face

 Dysarthria (difficult or unclear articulation of speech)

 Hemichorea

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Thalamo-Geniculate branch of PCA Internal Capsule Stroke

 The thalamogeniculate artery is a branch of the posterior cerebral artery supplying medial and lateral geniculate nucleus and the pulvinar nuclei of the thalamus.

 Suggestive clinical syndromes have been reported in unilateral infarcts in three territories. The infarcts in the thalamogeniculate pedicle territory are the most common ones, and typically produce a sensory stroke which may or may not evolve towards a Dejerine-Roussy syndrome.

 The infarcts in the posterior thalamo- subthalamic paramedian artery territory are often bilateral, because this artery is often a single branch coming off the basilar communicating artery.  When there are 2 arteries, the infarct is unilateral. It typically gives rise to decreased consciousness, neuropsychological impairment, and oculomotor disturbances, sometimes delayed abnormal movements.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Summary of Deep penetrating branches of Carotid a., ACA, MCA, PCA thalamus, internal capsule and basal ganglia

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Internal Capsule: Clinical Corner

 If a patient has weakness +/- sensory deficits, how can you tell whether the stroke is subcortical or cortical? What other symptoms or signs can help you localize the stroke to the internal capsule as opposed to the cortex?  A patient who presents with arm and leg weakness may have either a small internal capsule stroke or a large ACA + MCA cortical stroke. Looking at the homunculus in the figure above, the cortical leg area is supplied by the ACA and the arm area is supplied by the MCA. However, the injury to the cortices produces other symptoms and signs that not commonly produced by injury to the subcortical areas.  The presence of these cortical signs may exclude an internal capsule stroke:

 gaze preference or gaze deviation

 expressive or receptive aphasia

 visual field deficits

 visual or spatial neglect

 If any of these signs are present, the patient may have a cortical stroke, not an internal capsule stroke.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Posterior circulation strokes (Posterior Fossa) represent approximately 20% of all ischemic strokes. An in depth understanding of this area is Ischemic extremely important in the clinical setting due to the frequency of similar complaints so frequently Posterior seen in the office setting In contrast to the anterior circulation, several Circulation differences in presenting symptoms, clinical evaluation, diagnostic testing, and management strategy exist presenting a Stroke: challenge to the treating physician.

Ischemic Posterior Circulation Stroke: A Review Amre Nouh,1 Jessica Remke,2 and Sean of Anatomy, Clinical Ruland1,* Presentations, Diagnosis, and Current Management

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Ischemic Posterior Circulation Stroke:

 The posterior cerebral circulation (or simply, posterior circulation) is the blood supply to the posterior portion of the brain, including the occipital lobes, cerebellum and brainstem.

 The posterior circulation is supplied by the vertebral arteries that combine to form the basilar artery which then divides into the posterior cerebral arteries. From these main vessels, many smaller vessels supply the posterior structures of the brain, including:

 posterior inferior cerebellar artery

 anterior inferior cerebellar artery

 pontine branches

 superior cerebellar artery

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Does my dizzy patient have a stroke? Craniocervical pain Narrative reviews have suggested that craniocervical pain may accompany dizziness in patients with stroke in the posterior fossa because of the stroke itself (mass effect or direct involvement of pain-sensitive structures) or its underlying cause (e.g., dissection or aneurysm of the vertebral artery).22 Two studies addressed this issue. Headache or neck pain was present in a minority of patients presenting with acute vestibular syndrome . A statistically significant association was present with central causes (38% v. 12%, p < 0.05) was found in the larger study. 6. Kattah JC, Talkad AV, Wang DZ, et al. HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke 2009;40:3504–10 [PMC free article] [PubMed] [Google Scholar] 9. Norrving B, Magnusson M, Holtas S. Isolated acute vertigo in the elderly: Vestibular or vascular disease? Acta Neurol Scand 1995;91:43–8 [PubMed] [Google Scholar] 22. Edlow JA, Newman-Toker DE, Savitz SI. Diagnosis and initial management of cerebellar infarction. Lancet Neurol 2008;7:951–64 [PubMed] [Google Scholar] In another study Head pain occurs in 50–75% of all cases of vertebral artery dissection.

Larry E. Masula, D.C., DACNB, FAVRB, FAFICC 8/14/2019 117 A 65-year-old male presents with dizziness and generalized weakness early this evening while shopping after dinner. The patient recently underwent open heart surgery to have a prosthetic heart valve replace. He describes the dizziness as occurring gradually over the past few days without nausea or vomiting or ringing in the ears. On examination, the patient exhibits vertical nystagmus. A Dix-Hallpike was performed, which was negative for nystagmus or vertigo. Pneumatic insufflation of the tympanic membrane failed to provoke an episode of dizziness.

The patient’s gradual onset of vertigo, low intensity dizziness and the presence of only VERTICAL nystagmus is indicative of .midbrain or cerebellar pathology

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Common symptoms in the majority of brainstem These lesions are typically vascular in nature lesions include diplopia, dysarthria, vertigo but can be as result of other disorders such as nausea and vomiting. MS and pontine gliomas etc. ,

Clinical Aspects of Brainstem Disorders

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Signs and Symptoms of Vertebrobasilar Ischemia

Commit to memory the “5 D’s And 3 N’s”

Diplopia (or other visual problems)

Dysphagia

Drop attacks (sudden weakness in face/arm/ leg

Dizziness (vertigo, light-headedness, giddiness)

Dysarthria (slurred words or unable to speak = cranial nerve injury

Ataxia of gait (hemiparesis)

Nausea (possibly with vomiting)

Numbness (hemianesthesia)

Nystagmus

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC 2 Types Medullary Vascular Lesions

 There are typically only 2 kinds of medullary ischemic attacks, those that affect the Dorsal Lateral Medulla and the those that affect the Paramedian and Basal regions which are lumped together.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Brainstem Rule of 4

 The rule of 4 of the brainstem: a simplified method for understanding brainstem anatomy and brainstem vascular syndromes for the non- neurologist’.  Firstly, a quick review of the blood supply of the brainstem. Simply put the blood supply comes from:  1. paramedian branches  2. long circumferential branches (SAP)  superior cerebellar artery (SCA)  anterior inferior cerebellar artery (AICA)  posterior inferior cerebellar artery (PICA)

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Brainstem Rule of 4

 In the rule of 4 there are 4 rules  There are 4 structures in the ‘midline‘ beginning with M  There are 4 structures to the ‘side‘ (lateral) beginning with S  There are 4 cranial nerves in the medulla, 4 in the pons and 4 above the pons (2 in the midbrain)  There are 4 motor nuclei that are in the midline are those that divide equally into 12 except for 1 and 2, that is 3, 4, 6 and 12 (5, 7, 9 and 11 are in the lateral brainstem)

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Clinical Case: Your patient presents with the following:

 Vertigo, nausea and vomiting

 Ipsilateral facial pain and temperature loss

 Ipsilateral Horner’s

 Ataxia and dysmetria

 Weakness of palate, pharynx and larynx

 Dysphagia, hoarseness, diminished gag reflex

 Contralateral pain and temperature loss

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Lateral Medullary Stroke (Wallenberg)

This is the most common brainstem stroke. Dorsal lateral infarction causes damage referred to as a Wallenberg syndrome. Typically, you will have: Ipsilateral Horner’s syndrome, loss of pain and temperature over the face on the same side of the lesion. There can be cerebellar findings on the ipsilateral side causing ataxia. Contralateral loss of pain and temperature with.. You can get severe nausea, vomiting, vertigo, and nystagmus due to vestibular nuclei influence. Hiccups may be common do to lesion in the 9th and 10th nerves with difficulty swallowing.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Wallenberg Syndrome

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Medial Medullary Syndrome

Deviation of the tongue to the side of the infarct on attempted protrusion, caused by ipsilateral muscle weakness. Hypoglossal nerve fibers #8 on diagram Limb weakness (hemiplegia depending on severity), on the contralateral side of the infarct. Damage to medullary pyramids and hence to the corticospinal fibers of the pyramidal tract which cross over. #5 Loss of discriminative touch, conscious proprioception, and vibration sense on the contralateral side of the infarct (below the head) Damage to medial lemniscus # 6 on diagram

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Medial Medullary Syndrome The anteromedian part of the medulla is supplied by the vertebral artery, the rest of the medulla is supplied by PICA

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Pontine Vascular Syndromes

There are numerous pontine vascular syndromes (see below) of which we will only take a few minutes and review a few in the next few slides

 Caudal Basal Pontine Syndrome

 Locked-in Syndrome

 Medial Tegmental Pontine Syndrome

 Caudal Tegmental Pontine Syndrome

 One-and-a-Half Syndrome

 Rostral Basal Pontine Syndrome

 Dorsolateral Tegmental Pontine Syndrome

 Rostral Tegmental Syndrome

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC 3 Basic Pontine Vascular Lesions based on territory affected

 The same thing applies here as in A dorsal lateral lesion will give you a the medulla. probable Horner's syndrome, along with a loss of pain and temperature on  You can have the contralateral side.  dorsal lateral

 paramedian and If below mid-pontine level, you are  basal infarctions likely to have ipsilateral loss of facial sensation and some ipsilateral cerebellar involvement as well.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC 3 Pontine Vascular Lesions

 At mid-pontine level, the lateral  At lower pontine levels the pontine reticular formation will be vestibular nuclei and Cochlear involved causing a loss of lateral nuclei will be affected causing conjugate gaze towards the side of vestibular symptoms, nystagmus the lesion. Note: if both eyes are and deafness. This will frequently involved it is usually a pontine cause a loss of pain and disorder and if one eye is involved it temperature over the face and the is most likely an individual cranial opposite side of the body, Thus nerve. causing a crossed sensory loss. (see AICA syndrome)

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC 3 Pontine Vascular Lesions

A Pontine Paramedian infarction is identifiable at the level of the 6th nerve nucleus and will often cause a conjugate gaze palsy which is inability to move both eyes in a single horizontal (most commonly) or vertical direction

There may be damage to the 7th nerve as it sweeps around the 6:00 nerve nucleus, causing contralateral facial paralysis. If it extends far enough and clips the cortico spinal tracts the result is contralateral arm and leg paralysis.

If the medial lemniscus is damaged, you may lose touch and proprioception on the contralateral side of the body

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC 3 Pontine Vascular Lesions

Basal infarctions can be very complex and If a complete contralateral hemiplegia is have many aspects of involvement. present and there is ipsilateral 6th nerve damage and the eye will not abduct and ipsilateral 7th nerve damage causing facial Typically, there will be damage to the 6th and paralysis, this is called Millard Gubler 7th cranial nerve fascicles and damage to the syndrome pyramidal pathways as well.

If only the 6th nerve is affected with a contralateral hemiplegia, this is called Raymond’s syndrome

If the lesion is more lateral, then you may have loss in conjugate gaze, a Horner’s syndrome, deafness, facial numbness and facial palsy. this is called Foville’s syndrome

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Pontine lesions “Raymond’s Syndrome”

 Corticospinal tract involvement resulting in contralateral hemiplegia and 6th nerve damage.

 (A)(Raymond’s Syndrome-

 (B) Foville’s Syndrome further posterior than Millard-Gubler

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Foville’s Syndrome Inferior Medial Pontine Syndrome

Unilateral lesion in the dorsal pontine tegmentum in the caudal third of the pons

Structures affected by the infarct are the PPRF, nuclei of cranial nerves VI and VII, corticospinal tract, medial lemniscus, and the medial longitudinal fasciculus.

There's involvement of the fifth to eighth cranial nerves, central sympathetic fibers (Horner syndrome) and horizontal gaze palsy. If the lesion is more lateral then you may have loss of conjugate gaze a Horner’s syndrome, deafness, facial numbness and facial palsy

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Anterior Inferior Cerebellar Artery Syndrome (AICA)

Occlusion of AICA results in lateral pontine syndrome, also known as AICA syndrome. The symptoms include sudden onset vertigo and vomiting, nystagmus, falling to the side of the lesion (due to damage to vestibular nuclei), ipsilateral loss of sensation of the face (due to damage to principal sensory trigeminal nucleus), ipsilateral facial paralysis (due to damage to the facial nucleus) and ipsilateral hearing loss and tinnitus (due to damage to the cochlear nuclei). This the twin to a Wallenberg syndrome of the medulla with addition of hearing impairment by occluding the labyrinthine artery which is a branch of the AICA.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Labyrinthine Artery - Vascular Supply

It is important at this point to also review the clinically important Labyrinthine artery. 45% from AICA  24% superior cerebellar artery  16% basilar  Two divisions:

 anterior vestibular artery

 common cochlear artery  Vascular pathologies can give pulsatile tinnitus or deafness

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Mid Brain Lesions

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Mid Brain (Mesencephalon) Lesions

3 Areas are possible. Like the medulla and pons, these areas include:

Dorsolateral

Paramedian

Basal regions of the mesencephalon

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Nothnagel’s Syndrome

Dorsolateral Infarction. You will see a Horner's syndrome on the same side and total loss on the contralateral side of the body. You may have cerebellar deficit on the ipsilateral side due to damage of the superior cerebellar peduncle. You may have involvement of the ipsilateral 3rd nerve if extensive enough. A combination of ipsilateral cerebellar and 3rd nerve findings is called Nothnagel’s Syndrome.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Mesencephalon 3rd Nerve palsy

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Benedikt’s Syndrome

The next area that can be damage is the paramedian area . this will affect the ocular motor nucleus and an incomplete 3rd nerve lesion may occur. There may be disruption in the dentato- rubro-thalamo- cortical pathway Thus causing 3rd nerve findings on one side and cerebellar findings on the other.

 Specifically, the median zone is impaired. It can result from occlusion of the posterior cerebral artery or paramedian penetrating branches of the basilar artery.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Weber’s Syndrome, from the PCA can affect the mesencephalon

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Basilar Artery Syndrome

 Paramedian – wedge of pons in midline

 Short circumferential – lateral two thirds of pons and middle and superior peduncles

 Long circumferential – Superior and anterior inferior cerebellar

 Complete Basilar Artery occlusion (Locked in state) preserved consciousness, quadriplegia and cranial nerve signs

 Locked-in syndrome (LIS), also known as pseudocoma, is a condition in which a patient is aware but cannot move or communicate verbally due to complete paralysis of nearly all voluntary muscles in the body except for vertical eye movements and blinking.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Evaluating Stroke

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Cincinnati Stroke Scale

Interpretation: If any of the 3 signs are present, the probability of Stoke is 72%

Cincinnati Stroke Scale + (BEFAST) Balance: watch for a sudden loss of balance Eyes: is there a sudden loss of vision in one or both eyes? Or Diplopia Face: ask the person to smile. Does one side of the face droop? Speech: ask the person to repeat a simple phrase. Is the speech slurred or strange? Time: : if you observe any of these signs, call 9-1-1 immediately Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Acute Vestibular Syndrome (posterior circulation) H.I.N.T.S. to I.N.F.A.R.C.T. This is most likely the most common stroke patient to be seen in a chiropractic office due to their presenting symptoms

“H.I.N.T.S.” Battery  STROKE FINDINGS: “I.N.F.A.R.C.T.”

 Impulse Normal 1. Head Impulse Test  Fast-phase Alternating 2. Nystagmus  Re-fixation on Alternating Cover 3. Test of Skew Uncover Test

 Any ONE of these points to a Stroke

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Head Impulse Test

A normal patient in good health will not have nystagmus. If the patient suffers from a vestibulopathy such as a viral neuritis, the Head Impulse test will be abnormal because the eyes cannot remain focused on a target during the test. The eyes will appear to move back and forth. If you have a Peripheral Vestibular Nerve problem, you probably don’t have a brain problem. Abnormal finding is a GOOD finding because it it probably not a stroke.

What we are looking for is a Central Vestibular Syndrome. In this case there will be no dysmetric eye movements during the head impulse test and the eyes will remain fixed on the target. This is opposite of what you might think but the test is then considered to be negative. Note: this is also negative with a healthy patient whose eyes will not oscillate. So, this test must be correlated with all 3 parts of the HINTS battery. In this case of a stroke, the negative finding is a bad finding.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC 3. Head Impulse Test

 https://youtu.be/1q-VTKPweuk?t=295

Hold onto the patients skull

Patient fixates on examiners nose (or camera)

Move head back (maybe 20 degrees), Slowly to the right, then BRISKLY to midline. What you are looking for are catch-up Saccades of the eyes

In this video her eyes remain fixed on the camera = NORMAL or Abnormal?

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC 3. Head Impulse Test

 https://youtu.be/1q-VTKPweuk?t=324 Abnormal Notice that this man presents with nystagmus when he looks to the left and when his head is turned to the right. Do you see that there is a larger movement of the eyes from the right back to the mid line? That is an abnormal HIT which is reassuring which shows that he has a peripheral nerve problem and probably does not have a brain problem.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC 3. Head Impulse Test

 https://youtu.be/1q-VTKPweuk?t=389

 This lady has a rock-solid head impulse test. She is WORRISOME because she has acute vertigo and nystagmus and we cannot find a nerve problem.

 She probably has a BRAIN problem.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC H.I.N.T.S. Nystagmus Testing

 Performed in

 Primary Gaze

 Lateral Gaze

 In a normal volunteer there is No nystagmus in primary gaze. During lateral gaze some nystagmus may be considered normal.

 If the patient has a vestibulopathy, fixating the eyes on a target will suppress any nystagmus. This is not the case with a central lesion. So, during lateral gaze testing, learn to suppress any fixation by placing a piece of paper between their head and the wall and ask them to look at the wall as if the paper was not present. Otherwise, you might see nystagmus which would not be there without the sheet of paper.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC H.I.N.T.S. Nystagmus Testing

 https://youtu.be/1q-VTKPweuk?t=105

 Patient with vestibular neuritis. Note: here it is again, when he looks to the left see that the nystagmus increases. It is left beating and there is a rotatory component towards the left and it increases when he looks to the left and you can see the torsional component.

 When he looks to the right it lessens but the fast component is still towards the left.

 Unidirectional nystagmus, does not change direction and in this exam, it is reassuring and most likely a peripheral vestibular disorder.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC H.I.N.T.S. Nystagmus Testing

 https://youtu.be/1q-VTKPweuk?t=157 Compare to this lady who when she looks to the right, she has small horizontal nystagmus with the fast component to the right. Then, when she moves more central and to the left, you can see that the nystagmus beats towards the left. So, she has direction beating nystagmus or bidirectional nystagmus which is worrisome.

Note: nystagmus is named for the direction of the fast phase

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Cover / Uncover test

https://youtu.be/1q-VTKPweuk?t=201 2. H.I.N.T.S. Test of Skew • Examiner takes their hand and covers the eye and then (Vertical) quickly covers the other eye to observe if there is any vertical movement of the eye when it is uncovered.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC H.I.N.T.S. Test of Skew

 https://youtu.be/1q-VTKPweuk?t=214

 Observe that when the hand is taken away from the right eye, the eye will go medially and upward and when the examiners hand is taken away from the left eye it goes medially and downward.

 This abnormal skew deviation is worrisome

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC H.I.N.T.S. Test of Skew

 https://youtu.be/1q-VTKPweuk?t=214

 Observe that when the hand is taken away from the right eye, the eye will go medially and upward and when the examiners hand is taken away from the left eye it goes medially and downward.

 This abnormal skew deviation is worrisome

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC  Regarding patients who present to the ED with AIS, according to information cited in a review article published in Mayo Clinic Proceedings, “comorbidities are common in this patient population, with most patients having a history of hypertension and about one-third having diabetes mellitus. Peripheral, coronary, and other Evaluating Stroke arterial diseases are also common.”  For complete information, see:

 Hasan TF, Rabinstein AA, Middlebrooks EH, et al. Diagnosis and management of acute ischemic stroke. Mayo Clin Proc. 2018;93(4):523-538.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Evaluating Stroke

 “Observational studies have found that stroke risk increases 4 months before diagnosis of infective endocarditis. In some instances, the elevated risk is due to occult infective endocarditis,” according to information cited in a review article published in Mayo Clinic Proceedings.

 For complete information, see:

 Hasan TF, Rabinstein AA, Middlebrooks EH, et al. Diagnosis and management of acute ischemic stroke. Mayo Clin Proc. 2018;93(4):523-538.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Evaluating Stroke

 According to information cited in a review article published in Mayo Clinic Proceedings, in the ED “every patient with suspected acute stroke should have a focused neurologic examination yielding an NIHSS score,” but “the NIHSS is not a substitute for a full neurologic examination. Because of severity biases against nondominant [middle cerebral artery] and posterior circulation strokes, the NIHSS may be unreliable in assessing right hemisphere strokes due to large-volume infarct compared with left hemisphere strokes.”

 For complete information, see:

 Hasan TF, Rabinstein AA, Middlebrooks EH, et al. Diagnosis and management of acute ischemic stroke. Mayo Clin Proc. 2018;93(4):523-538.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Evaluating Stroke

 “Immediate brain imaging is an essential first step in managing patients with stroke. The American College of Radiology considers either CT angiography (CTA) or magnetic resonance angiography (MRA) to be appropriate,” according to information cited in a review article published in Mayo Clinic Proceedings.

 For complete information, see:

 Hasan TF, Rabinstein AA, Middlebrooks EH, et al. Diagnosis and management of acute ischemic stroke. Mayo Clin Proc. 2018;93(4):523-538.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Neuroimaging of silent cerebrovascular disease

 In a scientific statement published in Stroke, the AHA and ASA state regarding diagnosis of silent cerebrovascular disease by neuroimaging that “MRI has greater sensitivity than CT for diagnosis of silent cerebrovascular disease,” adding that, compared to CT, MRI “can better demonstrate and differentiate small cortical and subcortical infarction, lacunar infarcts, WMHs [white matter hyperintensities], perivascular spaces, brain atrophy, and other structural lesions.”  For complete information, see:  Smith EE, Saposnik G, Biessels GJ, Doubal FN, Fornage M, Gorelick PB, Greenberg SM, Higashida RT, Kasner SE, Seshadri S; on behalf of the American Heart Association Stroke Council; Council on Cardiovascular Radiology and Intervention; Council on Functional Genomics and Translational Biology; and Council on Hypertension. Prevention of stroke in patients with silent cerebrovascular disease: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2017;48:e44–e71. Accessed February 28, 2017.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Neuroimaging of silent cerebrovascular disease

 According to information cited in a scientific statement from the AHA and ASA published in Stroke, “most silent brain infarcts (80%–90%) are subcortical,” and “[a] minority of silent brain infarcts involve the cerebral cortex.”

 For complete information, see:

 Smith EE, Saposnik G, Biessels GJ, Doubal FN, Fornage M, Gorelick PB, Greenberg SM, Higashida RT, Kasner SE, Seshadri S; on behalf of the American Heart Association Stroke Council; Council on Cardiovascular Radiology and Intervention; Council on Functional Genomics and Translational Biology; and Council on Hypertension. Prevention of stroke in patients with silent cerebrovascular disease: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2017;48:e44–e71. Accessed February 28, 2017.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Neuroimaging of silent cerebrovascular disease

 According to information cited in a scientific statement from the AHA and ASA published in Stroke, “WMHs (white matter hyperintensities) of presumed vascular origin should be reported with the use of a validated visual rating scale such as the Fazekas scale for MRI.”  For complete information, see:  Smith EE, Saposnik G, Biessels GJ, Doubal FN, Fornage M, Gorelick PB, Greenberg SM, Higashida RT, Kasner SE, Seshadri S; on behalf of the American Heart Association Stroke Council; Council on Cardiovascular Radiology and Intervention; Council on Functional Genomics and Translational Biology; and Council on Hypertension. Prevention of stroke in patients with silent cerebrovascular disease: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2017;48:e44–e71. Accessed February 28, 2017.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Neuroimaging of silent cerebrovascular disease

 In a scientific statement published in Stroke, the AHA and ASA state “CMBs are visible on hemorrhage-sensitive MRI sequences but unapparent on CT.” Moreover, CMBs on MRI “appear as small, round, 5- to 10-mm areas of signal loss on MRI susceptibility-weighted sequences. They exhibit a blooming effect; that is, the diameter of the signal loss on the susceptibility-weighted sequence exceeds the actual size of the lesion,” and “there are potential mimics to avoid. Calcium deposits and vessels seen in cross section can have a similar appearance.”  For complete information, see:

 Smith EE, Saposnik G, Biessels GJ, Doubal FN, Fornage M, Gorelick PB, Greenberg SM, Higashida RT, Kasner SE, Seshadri S; on behalf of the American Heart Association Stroke Council; Council on Cardiovascular Radiology and Intervention; Council on Functional Genomics and Translational Biology; and Council on Hypertension. Prevention of stroke in patients with silent cerebrovascular disease: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2017;48:e44–e71. Accessed February 28, 2017.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Neuroimaging of silent cerebrovascular disease

 In a scientific statement published in Stroke, the AHA and ASA state that “WMHs become ubiquitous with advanced age” but “there is no clear scientific evidence for a threshold below which WMH can be considered entirely benign.”

 For complete information, see:

 Smith EE, Saposnik G, Biessels GJ, Doubal FN, Fornage M, Gorelick PB, Greenberg SM, Higashida RT, Kasner SE, Seshadri S; on behalf of the American Heart Association Stroke Council; Council on Cardiovascular Radiology and Intervention; Council on Functional Genomics and Translational Biology; and Council on Hypertension. Prevention of stroke in patients with silent cerebrovascular disease: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2017;48:e44–e71. Accessed February 28, 2017.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC  A review article published in The Medical Clinics of North America, Primary stroke discussing primary and secondary stroke prevention, states that prevention via “treatment of vascular risk factors is (common and uncommon) the most effective strategy for risk factor primary stroke prevention.” management  For complete information, see:  Caprio FZ, Sorond FA. Cerebrovascular disease: primary and secondary stroke prevention. Med Clin North Am. 2019;103(2):295-308.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Primary stroke prevention via risk factor management

 “Hypertension is the single most important modifiable risk factor for stroke; more than half of all strokes worldwide are attributed to hypertension,” according to information cited in a review article published in The Medical Clinics of North America.

 For complete information, see:

 Caprio FZ, Sorond FA. Cerebrovascular disease: primary and secondary stroke prevention. Med Clin North Am. 2019;103(2):295-308.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Primary stroke prevention via risk factor management

 According to data cited in a review article published in The Medical Clinics of North America, “potentially modifiable risk factors are associated with 90% of attributable risk for stroke worldwide; these include hypertension, smoking, obesity, diet, physical inactivity, diabetes, alcohol intake, psychosocial factors, cardiac disease, and apolipoprotein ratios.”

 For complete information, see:

 Caprio FZ, Sorond FA. Cerebrovascular disease: primary and secondary stroke prevention. Med Clin North Am. 2019;103(2):295-308.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Primary stroke prevention via risk factor management

 According to information cited in a review article published in The Medical Clinics of North America, “smoking is a leading modifiable risk factor for cerebrovascular disease, with a dose-dependent increase in ischemic and hemorrhagic strokes.”

 For complete information, see:

 Caprio FZ, Sorond FA. Cerebrovascular disease: primary and secondary stroke prevention. Med Clin North Am. 2019;103(2):295-308.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Primary stroke prevention via risk factor management

 According to information cited in a review article published in The Medical Clinics of North America, “primary stroke prevention in the general population is most successful when lifestyle modifications are made to lower multiple major risk factors. Cerebrovascular risk factors are additive and possibly compounding. For example, having 5 vascular risk factors may pose a similar 10-year risk as that of person with a prior stroke or MI.”

 For complete information, see:

 Caprio FZ, Sorond FA. Cerebrovascular disease: primary and secondary stroke prevention. Med Clin North Am. 2019;103(2):295-308.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Primary stroke prevention via risk factor management

 According to information cited in Stroke, “the evidence surrounding the association between iron status and stroke risk is conflicting. Several observational studies have found a link between low iron levels and an increased risk of stroke, whereas other studies support a link between higher iron status and an increased risk of stroke. Furthermore, some studies have identified no relationship between iron status and stroke risk.”

 For complete information, see:

 Gill D, Monori G, Tzoulaki I, Dehghan A. Iron status and risk of stroke: a Mendelian randomization study. Stroke. 2018;49(12):2815-2821.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Primary stroke prevention via risk factor management

 A study published in Stroke “investigated the association between iron status and stroke risk using MR and found that a higher iron status was associated with an increased risk of cardioembolic stroke.”

 For complete information, see:

 Gill D, Monori G, Tzoulaki I, Dehghan A. Iron status and risk of stroke: a Mendelian randomization study. Stroke. 2018;49(12):2815-2821.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Primary stroke prevention via risk factor management

 In the findings of an MR study published in Stroke, “there was no significant effect of iron status on risk of large artery stroke. Furthermore, for the 2 [single-nucleotide polymorphisms] available for small vessel stroke, neither was there any effect of iron status observed.”

 For complete information, see:

 Gill D, Monori G, Tzoulaki I, Dehghan A. Iron status and risk of stroke: a Mendelian randomization study. Stroke. 2018;49(12):2815-2821.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Primary stroke prevention via risk factor management

 Researchers state in Stroke that the MR study technique may be able “to investigate whether iron status also has a causal effect on risk of venous thromboembolism, which overlaps with cardioembolic stroke in the mechanism of thrombus formation, or indeed atrial fibrillation, which is the main risk factor for cardioembolic stroke.”

 For complete information, see:

 Gill D, Monori G, Tzoulaki I, Dehghan A. Iron status and risk of stroke: a Mendelian randomization study. Stroke. 2018;49(12):2815-2821.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Calcium & magnesium levels in intracranial bleeding

 According to information cited in Stroke, “both calcium and magnesium are involved in platelet function and the coagulation cascade.”

 For complete information, see:

 Can A, Rudy RF, Castro VM, et al. Low serum calcium and magnesium levels and rupture of intracranial aneurysms. Stroke. 2018;49(7):1747-1750.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Calcium & magnesium levels in intracranial bleeding

 According to information cited in Stroke, “recently, both hypocalcemia and hypomagnesemia have been significantly associated with extent of bleeding in patients with intracerebral hemorrhage.”

 For complete information, see:

 Can A, Rudy RF, Castro VM, et al. Low serum calcium and magnesium levels and rupture of intracranial aneurysms. Stroke. 2018;49(7):1747-1750.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Calcium & magnesium levels in intracranial bleeding

 Study findings, cited in Stroke, “demonstrated a relationship between low admission serum calcium levels and larger hematoma volume among patients with acute intracerebral hemorrhage. This finding was confirmed in another cohort study where hypocalcemia was associated with larger baseline intracerebral hemorrhage volumes and hematoma expansion.”

 For complete information, see:

 Can A, Rudy RF, Castro VM, et al. Low serum calcium and magnesium levels and rupture of intracranial aneurysms. Stroke. 2018;49(7):1747-1750.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Calcium & magnesium levels in intracranial bleeding

 In observational cohort study findings of patients with intracerebral hemorrhage, cited in Stroke, “lower magnesium levels at admission were associated with larger intracerebral hemorrhage volumes, hematoma growth, and worse functional outcome.

 For complete information, see:

 Can A, Rudy RF, Castro VM, et al. Low serum calcium and magnesium levels and rupture of intracranial aneurysms. Stroke. 2018;49(7):1747-1750.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Calcium & magnesium levels in intracranial bleeding

 Case-control study findings, published in Stroke, “showed that hypocalcemia and hypomagnesemia at diagnosis were significantly associated with ruptured [intracranial] aneurysms, which may be explained by impaired hemostasis.”

 For complete information, see:

 Can A, Rudy RF, Castro VM, et al. Low serum calcium and magnesium levels and rupture of intracranial aneurysms. Stroke. 2018;49(7):1747-1750.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Artificially-sweetened beverages and post- menopause stroke risk

 According to study findings published in Stroke, “self-reported consumption of ASBs was associated with increased risk of ischemic stroke, CHD, and all- cause mortality.”

 For complete information, see:

 Mossavar-Rahmani Y, Kamensky V, Manson JE, et al. Artificially sweetened beverages and stroke, coronary heart disease, and all-cause mortality in the Women’s Health Initiative. Stroke. 2019;50(3):555-562.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Artificially-sweetened beverages and post- menopause stroke risk

 Artificially-sweetened beverages and post-menopause stroke risk

 According to study findings published in Stroke, “self-reported consumption of ASBs was associated with increased risk of ischemic stroke, CHD, and all- cause mortality.”

 For complete information, see:

 Mossavar-Rahmani Y, Kamensky V, Manson JE, et al. Artificially sweetened beverages and stroke, coronary heart disease, and all-cause mortality in the Women’s Health Initiative. Stroke. 2019;50(3):555-562.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Artificially-sweetened beverages and post- menopause stroke risk

 Study findings identified “a positive association between higher intake of ASB (twice or more daily) and the incidence of ischemic stroke, in particular SAO [small artery occlusion] subtype,” as published in Stroke.

 For complete information, see:

 Mossavar-Rahmani Y, Kamensky V, Manson JE, et al. Artificially sweetened beverages and stroke, coronary heart disease, and all-cause mortality in the Women’s Health Initiative. Stroke. 2019;50(3):555-562.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Artificially-sweetened beverages and post-menopause stroke risk

 In women with no prior history of cardiovascular disease or diabetes mellitus, high consumption of ASB was associated with more than a 2-fold increased risk of small artery occlusion ischemic stroke,” according to findings of a longitudinal study of postmenopausal women in the US published in Stroke.

 For complete information, see:

 Mossavar-Rahmani Y, Kamensky V, Manson JE, et al. Artificially sweetened beverages and stroke, coronary heart disease, and all-cause mortality in the Women’s Health Initiative. Stroke. 2019;50(3):555-562.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Artificially-sweetened beverages and post-menopause stroke risk

 Within longitudinal study findings of postmenopausal women in the US, published in Stroke, “higher ASB consumption was significantly associated with higher ischemic stroke risk among blacks but not among whites or other race/ethnic groups.”

 For complete information, see:

 Mossavar-Rahmani Y, Kamensky V, Manson JE, et al. Artificially sweetened beverages and stroke, coronary heart disease, and all-cause mortality in the Women’s Health Initiative. Stroke. 2019;50(3):555-562.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Artificially-sweetened beverages and post-menopause stroke risk

 As published in Stroke, regarding a longitudinal study of postmenopausal women in the US, “[t]he finding that in women with BMI ≥30, high consumption of diet drinks was associated with an increased risk of all end points except hemorrhagic stroke in women is notable.”

 For complete information, see:

 Mossavar-Rahmani Y, Kamensky V, Manson JE, et al. Artificially sweetened beverages and stroke, coronary heart disease, and all-cause mortality in the Women’s Health Initiative. Stroke. 2019;50(3):555-562.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC  Motor learning is better if the methods are Principles of  Meaningful  Repetitive

Stroke  Intensive Rehabilitation  Task-Specific

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Improving Trunk control

 Focus on

 Trunk rotation, side flexion

 Combination movements, anterior and posterior weight shift . Begin sitting and progress to standing.

 Upper body-initiated shift patterns ( reaching and picking up objects)

 Balance and dynamic stabilization exercises

 Cycling and treadmill training

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Treatment Methods

 TENs  Activation all presynaptic pool input into the neuron (Activation)  Non-invasive brain stimulation  Identify and manage improper Fuel in  Mirror therapy the form of Dysglycemia,  Virtual reality training Hypoglycemia, Metabolic Syndrome, Insulin resistance. (Fuel - glucose)  Brain computer interface  Identify and manage anemia (Fuel –  SSRI O2)  Assure an adequate protein and fat intake  Identify and manage Inflammatory conditions, Infections and Autoimmunity

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Mirror Therapy

 There is increasing experimental evidence that some motor neural structures are recruited not only when actions are actually executed but also when the actions of another person are simply observed, or a movement is imagined.

 This forms of therapy is routinely used by athletes and dancers before a performance to reactivated in working memory the representation of a motor memory.

 The neurophysiological basis for this recruitment is associated with “mirror neurons”

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC CIMT (constraint induced movement therapy)

 The concept implies that by restricting the use of the unaffected upper extremity by a MIT or sling will force an individual to use the affected limb, to complete task-based activities, affecting neuroplastic change and improve upper extremity function over time.

 The aim is to overcome “learned nonuse” of the paretic limb

 The typical intervention consists of restricting the unaffected limb for 90% of waking hours for 14 days with 6 hours of therapy for 10 of those days.

 In the acute stage of stroke, high-intensity CIMT results in less improvement than low-intensity CIMT

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Noninvasive Brain Stimulation

 Noninvasive brain stimulation involves the application of weak electric or magnetic fields to the brain via the surface of the scalp with the goal of changing or normalizing brain activity

 Noninvasive brain stimulation modules brain excitability and functional plasticity with relative safety and facilitates motor learning when combined with a motor task

 2 most common forms are

 Transcranial direct current stimulation

 Transcranial magnetic stimulation

 Neither modality is FDA approved but both are currently being studies under off label research purposes.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Functional Neuromuscular Stimulation

 Peroneal nerve stimulation to aid foot dorsiflexion to clear the foot during the swing phase of walking can increase step length and walking speed in hemiparetic persons

 A growing number of commercial devices are available that use an accelerometer to switch on the below-knee stimulus

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC VR training

 Clinical trials also have revealed encouraging results for cognitive rehabilitation assessment and for the treatment of attention and spatial memory deficits and apraxia

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Exercises to overcome ocular injuries after stroke

 People often think of a stroke as having a profound effect on a victim’s motor functions—and it does. However, did you know that as many as two-thirds of stroke victims experience vision impairments as a result of a stroke? Not all visual impairments happen immediately after the stroke, but some victims will notice changes to their vision right away. Fortunately, like motor function, eye injuries can also improve following a stroke. With the help of specific eye- training exercises, you can rewire the brain to help improve eye functions. Like other stroke-rehabilitation methods, beginning eye exercises as soon as possible after stroke will give a better chance of recovering or improving sight.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Common Vision Problems

 There are a broad range of vision problems that can result after experiencing a stroke.

 The most common type of vision problem is loss of half of the visual field in each eye. Other types include loss of a quarter of the visual field or an island- like area of blindness.

 Additional vision problems include visual perception issues, caused by damage to the brain stem. This damage may result in double vision, dizziness, difficulties with depth and distance perception, difficulties with color detection and visual neglect.

 With visual neglect, certain objects in a stroke survivor’s field of vision are ignored.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC URMC / News / Retraining the Brain to See After Stroke New study details “physical therapy” for eyes Wednesday, April 12, 2017  Patients who went partially blind after suffering a stroke regained large swaths of rudimentary sight after undergoing visual training designed by researchers at the University of Rochester Medical Center’s Flaum Eye Institute.

 A new study out today in Neurology®, the medical journal of the American Academy of Neurology, provides the first evidence that rigorous visual training recovers basic vision in cortically blind patients with long-standing stroke damage in the primary visual cortex. Damage to this area of the brain prevents visual information from getting to other brain regions that help make sense of it, causing loss of sight in one-quarter to one-half of an individual’s normal field of view. Somewhere between 250,000 and 500,000 people suffer vision loss due to damage to the visual cortex each year.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Retraining the Brain to See After Stroke

 Huxlin, who is also a professor in the departments of Neuroscience, Brain & Cognitive Sciences and the Center for Visual Science at UR, developed a sort of physical therapy for the visual system – a way of rerouting visual information around the dead areas of the primary visual cortex.

 Her team created personalized software programs for 17 cortically blind patients that flashed small circles of striped patterns or moving dots in the patient’s blind field – the area of their field of view where they could no longer see. Patients reported the orientation of the stripes or the direction in which the dots were moving as they were flashed on the screen.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Eye Exercises to Help with Stroke Recovery

 Eye exercises are an important part of rehabilitation for stroke patients with visual impairments. They help strengthen the eye muscles for improved control to aid recovery from eye injuries after stroke. Here are a few eye exercises you can do at home:  Computer games. Download word search games to aid in visual perception. You can download word search games for free from several websites. Eye Can Learn and Lumosity also offer free games that can improve visual-tracking skills.  Transitioning exercises. Focus on an object close to you, and then look to an object farther away. Try to increase your speed looking between the two objects until you can go back and forth rapidly.  Tracking exercises. Have someone else hold a pencil in front of your face, about 18 inches from your eyes. Have the person move the pencil slowly, up and down and side to side, as you track it with your eyes. Remember to keep your head still and move only your eyes.

Larry E. Masula, D.C., FAVRB, FAFICC, FAFICC Thanks for taking Online Courses with Back To Chiropractic CE Seminars. I hope you enjoyed the course. Please feel free to provide feedback.

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