Signs of Central Nervous System Disorders

Total Page:16

File Type:pdf, Size:1020Kb

Signs of Central Nervous System Disorders C H A P T E R 2 SIGNS OF CENTRAL NERVOUS SYSTEM DISORDERS Disorders of the brain and the spinal cord – the two major objects by touch (stereognosis). Neurologists often components of the central nervous system (CNS) – typi- describe loss of those modalities as “cortical” sensory loss. cally cause readily recognizable combinations of paresis, Pain sensation, a “primary” sense, is initially received sensory loss, visual deficits, and neuropsychologic disor- by the thalamus, from which it is relayed to the cortex, ders (Box 2.1). Such signs of CNS disorders differ from limbic system, and elsewhere. Because the thalamus is those of the peripheral nervous system (PNS) and both situated above the brainstem but below the cerebral differ from the signs of psychogenic disorders. Neurolo- cortex, most patients with cerebral lesions still perceive gists formulate their preliminary diagnosis and often ini- painful stimuli. For example, patients with cerebral tiate treatment on the basis of the patient’s history and infarctions may be unable to specify a painful area of their the examination, but if results of investigations – such as body, but they will still feel the pain’s intensity and dis- laboratory testing or magnetic resonance imaging (MRI) comfort (see Chapter 14). – contradict the initial clinical impression, they will Visual loss of the same half-field in each eye, homony- usually revise or at least reconsider it. mous hemianopia (Fig. 2.7), is a characteristic sign of a contralateral cerebral lesion. Other equally characteristic visual losses are associated with lesions involving the eye, SIGNS OF CEREBRAL HEMISPHERE LESIONS optic nerve, or optic tract (see Chapters 4 and 12). Because they are situated far from the visual pathway, Hemiparesis, usually accompanied by changes in reflexes lesions in the brainstem, cerebellum, or spinal cord do and muscle tone, is one of neurology’s most prominent not cause visual field loss. and reliable signs. Damage to the corticospinal tract, also Another conspicuous sign of a cerebral hemisphere called the pyramidal tract (Fig. 2.1), in the cerebrum or lesion is focal (partial) or focal-onset seizures (see Chapter brainstem above (rostral to) the decussation of the pyra- 10). In fact, the majority of focal seizures that alter aware- mids, causes contralateral hemiparesis (Box 2.2) with ness or induce psychomotor phenomena originate in the weakness of the arm and leg – and, if the lesion is high temporal lobe. enough, the lower face – opposite the side of the lesion. Damage to this tract within the spinal cord causes ipsilat- eral arm and leg or only leg paresis, but no face paresis. Signs of Damage of the Dominant, The division of the motor system into upper and lower Nondominant, or Both Cerebral Hemispheres motor neurons is a basic construct of clinical neurology. During the corticospinal tract’s entire path from the Although hemiparesis, hemisensory loss, homonymous cerebral cortex to the motor cranial nerve nuclei and hemianopia, and focal seizures may result from lesions of the anterior horn cells of the spinal cord, this tract either cerebral hemisphere, several neuropsychologic consists of upper motor neurons (UMNs) (Fig. 2.2). The deficits are referable to either the dominant or nondomi- anterior horn cells, which are part of the PNS, begin nant hemisphere. Neurologists usually ask a patient’s the lower motor neuron (LMN). Cerebral lesions that handedness when taking a history, but if this information damage the corticospinal tract cause signs of UMN injury is unavailable, because approximately 85% of people (Figs. 2.2–2.5): are right-handed, they assume with reasonable confi- • Paresis with muscle spasticity dence that the left hemisphere serves as the dominant • Hyperactive deep tendon reflexes (DTRs) hemisphere. • Babinski signs. Lesions of the dominant hemisphere may cause lan- In contrast, PNS lesions, including motor neuron dis- guage impairment, aphasia, a prominent and frequently eases (diseases of the anterior horn cells) and disorders of occurring neuropsychologic deficit (see Chapter 8). nerves (neuropathy), cause signs of LMN injury: Because the corticospinal tract sits adjacent to the lan- • Paresis with muscle flaccidity and atrophy guage centers, right hemiparesis often accompanies • Hypoactive DTRs aphasia (see Fig. 8.1). • No Babinski signs. Lesions of the nondominant parietal lobe tend to Another indication of a cerebral lesion is loss of certain produce one or more striking neuropsychologic distur- sensory modalities over one half of the body, i.e., hemi- bances (see Chapter 8). For example, patients may neglect sensory loss (Fig. 2.6). A patient with a cerebral lesion or ignore left-sided visual and tactile stimuli (hemi- characteristically loses contralateral position sensation, inattention). They may fail to use their left arm and leg two-point discrimination, and the ability to identify because they neglect their limbs rather than because of 7 8 SECTION 1 CLASSIC ANATOMIC NEUROLOGY BOX 2.1 Signs of Common CNS Lesions Cerebral hemisphere* Hemiparesis with hyperactive deep tendon reflexes, spas- ticity, and Babinski sign Internal Hemisensory loss capsule Homonymous hemianopia Focal (partial) seizures Aphasia, hemi-inattention, and dementia Pseudobulbar palsy Basal ganglia* Movement disorders: parkinsonism, athetosis, chorea, and Midbrain hemiballismus Postural instability Rigidity Brainstem Cranial nerve palsy with contralateral hemiparesis Pons Internuclear ophthalmoplegia (MLF# syndrome) Nystagmus Bulbar palsy Cerebellum Tremor on intention^ Impaired rapid alternating movements (dysdiadocho- kinesia)^ Medulla Ataxic gait Scanning speech Spinal cord Paraparesis or quadriparesis Spasticity Spinal cord Sensory loss up to a “level” Bladder, bowel, and sexual dysfunction FIGURE 2.1 ■ Each corticospinal tract originates in the cerebral *Signs contralateral to lesions cortex, passes through the internal capsule, and descends into #MLF, Medial longitudinal fasciculus the brainstem. The tracts cross in the pyramids, which are pro- ^Signs ipsilateral to lesions tuberances on the inferior portion of the medulla, to descend in the spinal cord mostly as the lateral corticospinal tract. The corticospinal tracts synapse with the anterior horn cells of the spinal cord, which give rise to peripheral nerves. Neurologists BOX 2.2 Signs of Common Cerebral Lesions often call the corticospinal tract the pyramidal tract because it crosses in the pyramids. The extrapyramidal system, which Either hemisphere* modulates the corticospinal tract, originates in the basal ganglia and cerebellum, and remains within the brain. Hemiparesis with hyperactive deep tendon reflexes and a Babinski sign Hemisensory loss Homonymous hemianopia damage produces several important disturbances that Focal seizure Dominant hemisphere psychiatrists are likely to encounter in their patients. One Aphasia: fluent, nonfluent, conduction, or isolation of them, pseudobulbar palsy, best known for producing Gerstmann syndrome: acalculia, agraphia, finger agnosia, emotional lability, results from bilateral corticobulbar tract and left–right confusion damage (see Chapter 4). The corticobulbar tract, like its Alexia without agraphia counterpart the corticospinal tract, originates in the Nondominant hemisphere motor cortex of the posterior portion of the frontal lobe. Hemi-inattention It innervates the brainstem motor nuclei, which in turn Anosognosia innervate the head and neck muscles. Traumatic brain Constructional apraxia injury (TBI), multiple cerebral infarctions (strokes), and Both hemispheres frontotemporal dementia (see Chapter 7), are apt to Dementia Pseudobulbar palsy strike the corticobulbar tract, as well as the surrounding frontal lobes, and thereby cause pseudobulbar palsy. *Signs contralateral to lesions Damage to both cerebral hemispheres – from large or multiple discrete lesions, degenerative diseases, or meta- bolic abnormalities – also causes dementia (see Chapter paresis. When they have left hemiparesis, patients may 7). In addition, because CNS damage that causes demen- not appreciate it (anosognosia). Many patients lose their tia must be extensive and severe, it usually also produces ability to arrange matchsticks into certain patterns or at least subtle physical neurologic findings, such as hyper- copy simple forms (constructional apraxia, Fig. 2.8). active DTRs, Babinski signs, mild gait impairment, and As opposed to signs resulting from unilateral cerebral frontal lobe release reflexes. However, many neurode- hemisphere damage, bilateral cerebral hemisphere generative illnesses that cause dementia, particularly 2 SIGNS OF CENTRAL NERVOUS SYSTEM DISORDERS 9 A UMN Brain Normal UMN lesions Spinal cord B Afferent limb C LMN LMN LMN efferent Peripheral nerve lesion limb Quadriceps muscle tendon ∅ ∅ A B C FIGURE 2.2 ■ A, Normally, when neurologists strike a patient’s quadriceps tendon with a percussion hammer, the maneuver elicits a DTR. In addition, when they stroke the sole of the foot to elicit a plantar reflex, the big toe bends downward (flexes). B, When brain or spinal cord lesions injure the corticospinal tract, producing upper motor neuron (UMN) damage, DTRs react briskly and forcefully, i.e., DTRs are hyperactive. As another sign of UMN damage, the plantar reflex is extensor (a Babinski sign). C, In contrast, peripheral nerve injury causes lower motor neuron (LMN) damage, the DTR is hypoactive and the plantar reflex is absent. FIGURE 2.3 ■ This patient shows right hemiparesis with weak-
Recommended publications
  • A Syndrome-Based Clinical Approach for Clerkship Students General Comments 1. This Is Not an All-Inclusive “Cookbook” for Ev
    A Syndrome-Based Clinical Approach for Clerkship Students General Comments 1. This is not an all-inclusive “cookbook” for every Neurology patient, but a set of guidelines to help you rationally approach patients with certain syndromes (sets of signs and symptoms which suggest a lesion in particular parts of the nervous system). 2. As you obtain a history and perform a neurological physical exam, try initially to localize all the patient’s signs and symptoms to one, single lesion in the nervous system. It may be surprising that a variety of signs and symptoms, at first glance apparently unrelated, on second thought can localize accurately to a single lesion. If this approach fails, then consider multiple, separate lesions for the patient’s signs and symptoms. 3. The tempo or rate at which signs and symptoms develop or occur often suggests the underlying pathological process. a. sudden onset---favors stroke (ischemia or hemorrhage), seizure, migraine (or other headache syndromes), and trauma b. subacute onset---favors inflammatory, infectious or immune-mediated disorders c. chronic onset---favors degenerative disorders, tumors Toximetabolic disorders, potentially treatable and reversible, may mimic lesions in the nervous system, and can evolve at variable tempos. Hereditary conditions may be congenital (present at birth) and nonprogressive or static, or develop later in life, with variable rates of progression. Family members affected by the same genetic disorder may be remarkably similar with regards to onset and clinical severity, while some genetic disorders vary widely regarding when and how severely family members are affected. 4. In the central nervous system, “positive symptoms or phenomena,” such as flashes of light, or a tingling sensation, suggest “excitation” or increased activity in the nervous system: migraine or seizure.
    [Show full text]
  • Inherited Neuropathies
    407 Inherited Neuropathies Vera Fridman, MD1 M. M. Reilly, MD, FRCP, FRCPI2 1 Department of Neurology, Neuromuscular Diagnostic Center, Address for correspondence Vera Fridman, MD, Neuromuscular Massachusetts General Hospital, Boston, Massachusetts Diagnostic Center, Massachusetts General Hospital, Boston, 2 MRC Centre for Neuromuscular Diseases, UCL Institute of Neurology Massachusetts, 165 Cambridge St. Boston, MA 02114 and The National Hospital for Neurology and Neurosurgery, Queen (e-mail: [email protected]). Square, London, United Kingdom Semin Neurol 2015;35:407–423. Abstract Hereditary neuropathies (HNs) are among the most common inherited neurologic Keywords disorders and are diverse both clinically and genetically. Recent genetic advances have ► hereditary contributed to a rapid expansion of identifiable causes of HN and have broadened the neuropathy phenotypic spectrum associated with many of the causative mutations. The underlying ► Charcot-Marie-Tooth molecular pathways of disease have also been better delineated, leading to the promise disease for potential treatments. This chapter reviews the clinical and biological aspects of the ► hereditary sensory common causes of HN and addresses the challenges of approaching the diagnostic and motor workup of these conditions in a rapidly evolving genetic landscape. neuropathy ► hereditary sensory and autonomic neuropathy Hereditary neuropathies (HN) are among the most common Select forms of HN also involve cranial nerves and respiratory inherited neurologic diseases, with a prevalence of 1 in 2,500 function. Nevertheless, in the majority of patients with HN individuals.1,2 They encompass a clinically heterogeneous set there is no shortening of life expectancy. of disorders and vary greatly in severity, spanning a spectrum Historically, hereditary neuropathies have been classified from mildly symptomatic forms to those resulting in severe based on the primary site of nerve pathology (myelin vs.
    [Show full text]
  • Ataxic Gait in Essential Tremor: a Disease-Associated Feature?
    Freely available online Reviews Ataxic Gait in Essential Tremor: A Disease-Associated Feature? Ashwini K. Rao1* & Elan D. Louis2 1Department of Rehabilitation & Regenerative Medicine (Program in Physical Therapy), G.H. Sergievsky Center, Huntington's Disease Center of Excellence, Center of Excellence in Alzheimer's Disease, Columbia University, New York, NY, USA, 2Department of Neurology and Epidemiology (Chronic Diseases); Chief, Division of Movement Disorders, Co-Director- Center for Neuroepidemiology and Clinical Neurology Research, New Haven, CT, USA Abstract Background: While accumulating evidence suggests that balance and gait impairments are commonly seen in patients with essential tremor (ET), questions remain regarding their prevalence, their relationship with normal aging, whether they are similar to the impairments seen in spinocerebellar ataxias, their functional consequences, and whether some ET patients carry greater susceptibility. Methods: We conducted a literature search (until December 2018) on this topic. Results: We identified 23 articles on gait or balance impairments in ET. The prevalence of balance impairment (missteps on tandem walk test) was seven times higher in ET patients than controls. Gait impairments in ET included reduced speed, increased asymmetry, and impaired dynamic balance. While balance and gait problems worsened with age, ET patients were more impaired than controls, independent of age. The pattern of impairments seen in ET was qualitatively similar to that seen in spinocerebellar ataxias. Balance and gait impairments resulted in greater number of near falls in ET patients. Factors associated with balance and gait impairments in ET included age, presence of tremor in midline structures, and cognitive dysfunction. Discussion: Accumulating evidence suggests that balance and gait impairments are common in ET patients and occur to a greater extent in controls.
    [Show full text]
  • THE NEUROLOGY Exam & Clinical Pearls
    THE NEUROLOGY Exam & Clinical Pearls Gaye McCafferty, RN, MS, NP-BC, MSCS, SCRN NPANYS-SPHP Education Day Troy, New York April 7, 2018 Objectives I. Describe the core elements of the neurology exam II. List clinical pearls of the neuro exam Neurology Exam . General Physical Exam . Mental Status . Cranial Nerves . Motor Exam . Reflex Examination . Sensory Exam . Coordination . Gait and Station 1 General Systemic Physical Exam Head Trauma Dysmorphism Neck Tone Thyromegaly Bruits MSOffice1 General Systemic Physical Exam .Cardiovascular . Heart rate, rhythm, murmur; peripheral pulses, JVD .Pulmonary . Breathing pattern, cyanosis, Mallampati airway .General Appearance Hygiene, grooming, weight (signs of self neglect) .Funduscopic Exam Mental Status Level of Consciousness . Awake . Drowsy . Somnolent . Comatose 2 Slide 5 MSOffice1 , 6/14/2009 Orientation & Attention . Orientation . Time . Place . Person Orientation & Attention . Attention . Digit Span-have the patient repeat a series of numbers, start with 3 or 4 in a series and increase until the patient makes several mistakes. Then explain that you want the numbers backwards. Normal-seven forward, five backward Hint; use parts of telephone numbers you know Memory Immediate recall and attention Tell the patient you want him to remember a name and address – Jim Green – 20 Woodlawn Road, Chicago Note how many errors are made in repeating it and how many times you have to repeat it before it is repeated correctly. Normal: Immediate registration 3 Memory . Short-term memory . About 5 minutes after asking the patient to remember the name and address, ask him to repeat it. Long –term memory . Test factual knowledge . Dates of WWII . Name a president who was shot dead Memory Mini-Mental State Exam – 30 items Mini-Cog – Rapid Screen for Cognitive Impairment – A Composite of 3 item recall and clock drawing – Takes about 5 minutes to administer Mini-Cog Mini-Cog Recall 0 Recall 1-2 Recall 3 Demented Non-demented Abnormal Clock Normal Clock Demented Non-demented 4 Memory .
    [Show full text]
  • Depression Prevalence in Postgraduate Students and Its Association with Gait Abnormality
    SPECIAL SECTION ON DATA-ENABLED INTELLIGENCE FOR DIGITAL HEALTH Received November 7, 2019, accepted November 21, 2019, date of publication December 2, 2019, date of current version December 16, 2019. Digital Object Identifier 10.1109/ACCESS.2019.2957179 Depression Prevalence in Postgraduate Students and Its Association With Gait Abnormality JING FANG 1, TAO WANG 2, (Student Member, IEEE), CANCHENG LI 2, XIPING HU 1,2, (Member, IEEE), EDITH NGAI 3, (Senior Member, IEEE), BOON-CHONG SEET 4, (Senior Member, IEEE), JUN CHENG 1, YI GUO 5, AND XIN JIANG 6 1Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, China 2School of Information Science and Engineering, Lanzhou University, Gansu 730000, China 3Department of Information Technology, Uppsala University, Uppsala 75105, Sweden 4Department of Electrical and Electronic Engineering, Auckland University of Technology, Auckland 1010, New Zealand 5Department of Neurology, Shenzhen People's Hospital, Second Clinical Medical College of Jinan University, First Affiliated Hospital of Southern University of Science and Technology, Shenzhen 518020, China 6Department of Geriatrics, Shenzhen People's Hospital, Second Clinical Medical College of Jinan University, First Affiliated Hospital of Southern University of Science and Technology, Shenzhen 518020, China Corresponding authors: Xiping Hu ([email protected]) and Xin Jiang ([email protected]) This work was supported in part by Shenzhen Technology under Project JSGG20170413171746130, in part by the National Natural Science Foundation of China under Grant 61632014, Grant 61802159, Grant 61210010, Grant 61772508, and Grant 61402211, and in part by the Program of Beijing Municipal Science and Technology Commission under Grant Z171100000117005. ABSTRACT In recent years, an increasing number of university students are found to be at high risk of depression.
    [Show full text]
  • Gait Disorders in Older Adults
    ISSN: 2469-5858 Nnodim et al. J Geriatr Med Gerontol 2020, 6:101 DOI: 10.23937/2469-5858/1510101 Volume 6 | Issue 4 Journal of Open Access Geriatric Medicine and Gerontology STRUCTURED REVIEW Gait Disorders in Older Adults - A Structured Review and Approach to Clinical Assessment Joseph O Nnodim, MD, PhD, FACP, AGSF1*, Chinomso V Nwagwu, MD1 and Ijeoma Nnodim Opara, MD, FAAP2 1Division of Geriatric and Palliative Medicine, Department of Internal Medicine, University of Michigan Medical School, USA Check for 2Department of Internal Medicine and Pediatrics, Wayne State University School of Medicine, USA updates *Corresponding author: Joseph O Nnodim, MD, PhD, FACP, AGSF, Division of Geriatric and Palliative Medicine, Department of Internal Medicine, University of Michigan Medical School, 4260 Plymouth Road, Ann Arbor, MI 48109, USA Abstract has occurred. Gait disorders are classified on a phenom- enological scheme and their defining clinical presentations Background: Human beings propel themselves through are described. An approach to the older adult patient with a their environment primarily by walking. This activity is a gait disorder comprising standard (history and physical ex- sensitive indicator of overall health and self-efficacy. Impair- amination) and specific gait evaluations, is presented. The ments in gait lead to loss of functional independence and specific gait assessment has qualitative and quantitative are associated with increased fall risk. components. Not only is the gait disorder recognized, it en- Purpose: This structured review examines the basic biolo- ables its characterization in terms of severity and associated gy of gait in term of its kinematic properties and control. It fall risk. describes the common gait disorders in advanced age and Conclusion: Gait is the most fundamental mobility task and proposes a scheme for their recognition and evaluation in a key requirement for independence.
    [Show full text]
  • Direct Anterior Total Hip Arthroplasty Gait Biomechanics at Three and Six Months Post Surgery
    DIRECT ANTERIOR TOTAL HIP ARTHROPLASTY GAIT BIOMECHANICS AT THREE AND SIX MONTHS POST SURGERY A THESIS SUBMITTED TO THE GRADUATE DIVISION OF THE UNIVERSITY OF HAWAI’I IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF MASTER OF SCIENCE IN KINESIOLOGY AND REHABILITATION SCIENCE AUGUST 2012 By: Ryan J. Moizon Thesis Committee: Iris Kimura, Chairperson Ronald Hetzler Christopher Stickley Keywords: Total hip arthroplasty; kinematics; kinetics TABLE OF CONTENTS List of Tables ii List of Figures iii Part I Introduction 1 Methods 4 Results 7 Discussion 12 Partil Review of literature 19 Appendix A: Data Collection Forms 37 Appendix B: Health History Form 40 Appendix C: WWB THA Informed Consent Form 42 Appendix D: WRB Control Informed Consent Form 53 Appendix F: Control Flyer 62 References 64 LIST OF TABLES Table Page 1. Demographic Data: Means and Standard Deviations for DA THA and Control group 7 2. Walking Velocity: Means and Standard Deviations for DA THA and Control group $ 3. Kinematic Variables: Mean and standard deviations for DA THA and Control group 9 4. Kinetic Variables: Mean and standard deviations for DA-THA and Control groups 11 5. Maximum VGRF: Means and Standard Deviations for DA THA and Control groups 11 LIST OF FIGURES Figure Page 1. Mean Values for Walking Velocity for DA THA and Control groups at initial test, 3 and 6 months post-test 13 2. Mean Values for Hip FlexionlExtension Excursion for DA THA and Control groups at initial test, 3 and 6 months post-test 14 3. Mean Values for Maximum VGRF for DA THA and Control groups at initial test, 3 and 6 months post-test 15 4.
    [Show full text]
  • Abnormality of Gait As a Predictor of Non-Alzheimer Dementia
    GAIT ABNORMALITY AND NON-ALZHEIMER’S DEMENTIA ABNORMALITY OF GAIT AS A PREDICTOR OF NON-ALZHEIMER’S DEMENTIA JOE VERGHESE, M.D., RICHARD B. LIPTON, M.D., CHARLES B. HALL, PH.D., GAIL KUSLANSKY, PH.D., MINDY J. KATZ, M.P.H., AND HERMAN BUSCHKE, M.D. ABSTRACT syndromes account for 30 to 50 percent of cases in Background Neurologic abnormalities affecting elderly patients who present for evaluation of abnor- gait occur early in several types of non-Alzheimer’s de- mal gait.2-5 Like the frequency of gait disorders, the mentias, but their value in predicting the development prevalence of dementia also increases with age.6 Al- of dementia is uncertain. though Alzheimer’s disease is the most common type Methods We analyzed the relation between neuro- of dementia, vascular and other non-Alzheimer’s de- logic gait status at base line and the development of mentias account for 30 to 50 percent of all cases of de- dementia in a prospective study involving 422 sub- mentia.6-9 The prevalence of vascular dementia is high jects older than 75 years of age who lived in the com- worldwide and is particularly high in Asia.6,9 Patients munity and did not have dementia at base line. Cox with vascular dementia may be more depressed, have proportional-hazards regression analysis was used to calculate hazard ratios with adjustment for potential greater functional impairment, and require different confounding demographic, medical, and cognitive diagnostic and therapeutic approaches than patients variables. with Alzheimer’s disease.10 Recent studies have fo- Results
    [Show full text]
  • Understanding and Treating Gait Abnormality in Dravet Syndrome
    Understanding and treating gait abnormality in Dravet syndrome Anne Stratton, MD, FAAP, FAAPMR Biennial Dravet Syndrome Foundation Family and Professional Conference July 19-22, 2018 Disclosures I have no financial or personal disclosures relevant to any information in this talk Objectives Review the following factors associated with gait decline in Dravet syndrome Characteristic gait abnormalities Review physical changes Review the timing of onset of gait changes Touch on the possible etiology of gait changes Discuss functional implications Discuss treatment options Characteristic gait abnormalities Ataxia Impaired cerebellar function and joint proprioception Impaired awareness of body position in space Impaired balance: “drunken sailor” Crouch Excessive hip, knee and ankle flexion Inefficient pattern “Sinking into the floor” Bradykinesia/ parkinsonism Slowed movements Decreased initiation “Shuffling, freezing” Spasticity Increased muscle tone, jerky, tight muscles Physical changes Femoral anteversion Hip flexion Knee flexion Tibial lateral torsion Pes planovalgus Hip dysplasia Scoliosis Flexion at hips Internal femoral rotation Flexion at knees External tibial rotation Collapse of arch Timing of onset of changes 0-5 years: Gait pattern: some variability, mostly within normal limits Bony abnormalities: foot deformity develops, some hip internal rotation 6-12 years: Gait pattern: some early crouch characteristics Bony abnormalities: foot deformity, tibial torsion, scoliosis 13+ years: Gait pattern:
    [Show full text]
  • GAIT DISORDERS, FALLS, IMMOBILITY Mov7 (1)
    GAIT DISORDERS, FALLS, IMMOBILITY Mov7 (1) Gait Disorders, Falls, Immobility Last updated: April 17, 2019 GAIT DISORDERS ..................................................................................................................................... 1 CLINICAL FEATURES .............................................................................................................................. 1 CLINICO-ANATOMICAL SYNDROMES .............................................................................................. 1 CLINICO-PHYSIOLOGICAL SYNDROMES ......................................................................................... 1 Dyssynergy Syndromes .................................................................................................................... 1 Frontal gait ............................................................................................................................ 2 Sensory Gait Syndromes .................................................................................................................. 2 Sensory ataxia ........................................................................................................................ 2 Vestibular ataxia .................................................................................................................... 2 Visual ataxia .......................................................................................................................... 2 Multisensory disequilibrium .................................................................................................
    [Show full text]
  • Relationship Between Essential Tremor and Cerebellar Dysfunction According to Age
    Journal of Clinical Neurology / Volume 1 / April, 2005 Original Articles Relationship Between Essential Tremor and Cerebellar Dysfunction According to Age Eui-Seong Lim, M.D., Man-Wook Seo, M.D., Seong-Ryong Woo, M.D., Suk-Young Jeong, M.D., Seul-Ki Jeong, M.D. Department of Neurology, Chonbuk National University College of Medicine, Jeonju, Korea Background: The cerebellum and its neural circuitry have been assumed to play a major role in the pathophysiology of essential tremor (ET). In this study, we sought to find associations between ET and cerebellar dysfunction. Methods: We performed tandem gait test in 41 ET patients and 44 age-matched controls. Investigators assessed tandem gait by counting the number of missteps during ten-step tandem walk and each subject repeated the trial three times. Results: ET patients had a higher average and total numbers of missteps during tandem gait tests than control subjects (p<0.05). Sex-adjusted odds ratio of the association between tandem gait abnormality and ET was 3.40 (95% confidence intervals 1.06-10.85). According to age stratification, aged ET patients (age ≥70 years) showed significantly higher prevalence of tandem gait abnormality than young ones. Interaction terms determined by a likelihood ratio test was also statistically significant (p<0.05). Conclusions: Dysfunction of cerebellar neural circuitry may be associated with the pathophysiological mechanism of ET. In addition, aging may be an important factor modifying the association. J Clin Neurol 1(1):76-80, 2005 Key Words : Essential tremor, Tandem gait, Cerebellum, Age INTRODUCTION assumed to play a major role in the pathophysiology of ET.3 To date, a functional disturbance of olivocerebellar circuit is the most popular hypothesis for the etiology of Essential tremor (ET) is one of the most common ET.4 Positron emission tomography (PET) studies have movement disorders.
    [Show full text]
  • Evaluating the Child with Unsteady Gait
    Review Article Evaluating the child with unsteady gait Mohammed M. Jan, MBChB, FRCP(C). ABSTRACT From the Department of Pediatrics, King Abdul-Aziz University Hospital, Jeddah, Kingdom of Saudi Arabia. Address correspondence and reprint request to: Prof. Mohammed M. S. Jan, Department of Pediatrics, King Abdul-Aziz University يعتبر خلل التوازن أثناء املشي من اﻷعراض الشائعة لدى اﻷطفال Hospital, PO Box 80215, Jeddah 21589, Kingdom of Saudi (Arabia. Tel. +996 (2) 6401000 Ext. 20208. Fax. +996 (2 بقسم الطوارئ واﻷعصاب. تتعدد أسباب خلل التوازن، ولكن E-mail: [email protected] .6403975 من أهم اولويات التقييم اﻷولى هو التأكد من عدم وجود التهاب أو ورم بالدماغ. التعرف علي املسببات احلميدة والغير عصبية ًأيضا eurological disorders are common in Saudi Arabia مهم لتفادى القيام بفحوصات متعددة دون احلاجة إليها أو تنومي Naccounting for up to 30% of all consultations to املريض باملستشفى. في هذه املقالة النقدية نقدم مراجعة حديثة pediatrics.1 Trauma, ingestion, and acute neurological عن تقييم الطفل املصاب بخلل التوازن مع مناقشة الفحوصات disorders are common, mainly as a result of improper الﻻزمة والعﻻج. قد يكون خلل التوازن ناجت عن مرض باملخيخ safety practices of many parents.2 Consanguineous أو مشكلة حسية، ًعلما بأن أمراض املخيخ قد تكون حادة، marriages also add to the problem, resulting in مزمنة، متدهورة، أو متقطعة. وتتعدد أسباب هذه املشكلة و increased prevalence of many inherited and genetic منها اﻹصابات، اﻻلتهابات، أمراض اﻻستقﻻب، العيوب اخللقية، neurological disorders.3,4 Unsteadiness and ataxia are واﻷورام. أما أسباب خلل التوازن الناجت عن مشاكل اﻹحساس relatively common neurological presentations of a فيكون بسبب تأثر في اﻷعصاب الطرفية أو احلبل الشوكي.
    [Show full text]