4 Disturbances in Consciousness and Epilepsy
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4 Disturbances in Consciousness and Epilepsy 4.1 Approach to Disturbances of Consciousness 4.1.1 Faints and Fits Clear Hx most important Important to differentiate between: □ Vertigo: abnormal perception of movement □ Unsteadiness: ataxia, proprioception, weakness53, visual disturbance, joint diseases… □ Lightheadedness: presyncope, syncope, hypoglycaemia, anxiety, hyperventilation, panic attack, psychogenic non-epileptic attacks □ Epilepsy Loss of consciousness (LOC) only occurs in the last two categories □ Suggests a generalized dysfunction of the brain D/dx Syndrome Mechanism Features Causes - Neurocardiogenic (autonomic - Preceded by brief feeling of lightheadedness reflex-related): (presyncope) Situational, eg. - LOC typically for <1min micturition Generalized - Associated S/S: darkening of vision, tinnitus, Vasovagal Syncope hypoperfusion hyperventilation, distal tingling, nausea, Hypertensive carotid to the brain clamminess or sweating sinus syndrome - Recovery quick and without confusion Postural hypotension - Often precipitated by pain, emotion or standing - Cardiogenic (insufficient CO): position Arrhythmia LV outflow obstruction - May be preceded by aura (eg. peculiar taste/smell, déjà vu feeling, auditory hallucination, anxiety, nausea, abdominal pain) - Course varies according to type - Epilepsy54 - LOC, falling + clonic movements (generalized - Secondary causes: congenital, Electric tonic-clonic) Seizure dysfunction - LOC + staring w/o movement (absence) hydrocephalus, hypoxia, drugs, of the brain - Localized contractions ± LOC (focal) toxins, metabolic, infective, - LOC typically lasts >1 min inflammatory, degenerative - Associated with incontinence and tongue-biting - Recovery slow with prolonged confusion, headache and focal neurological signs - Episodes often prolonged, sometimes >30min - Specific emotional trigger Pseudo- Psychogenic - Partially retained awareness - Psychogenic (~10% of LOC) seizure - Rapid recovery or subsequent emotional distress - Tongue biting, incontinence unlikely but possible Toxic/ Toxic - Transient, intermittent coma - Alcohol, solvents, barbituates 53 Sudden weakness due to TIAs may result in sudden collapse, but the patient should not suffer from any LOC. 54 Seizure is the symptom, epilepsy is the tendency to have recurrent seizures. - Page 76 of 179 - Metabolic - LOC - Insulin coma Metabolic - Often preceded by sweating, weakness, confusion - Oral hypoglycaemic Hx Obtain Hx from both pt and informant Hx from pt: Common forms of aura: □ Context: - Peculiar taste or smell → During blood-taking, micturition (syncope) - Feeling of déjà vu → During sleep (seizure) - Feeling of jamais vu → Standing (orthostatic hypotension) - Hearing of familiar music → During exercise (outflow obstruction) - Feeling of fear or anxiety welling up in chest □ Prodrome: - Visceral feelings, eg. nausea, → Aura (seizure) abdominal pain → Light-headedness, sweatiness, visual fading (syncope) □ Recovery: → Rapid (syncope) → Gradual with drowsiness (seizure) □ Associated: tongue-biting, incontinence (seizure) □ Drug history Hx from informants: □ Duration: <1min (syncope), >1min (seizure), >30min (psychogenic) □ Movement: → Brief, asynchronous jerking (syncope) → More prolonged synchronous tonic-clonic movement (seizure) □ Colour changes: pallor (syncope), cyanotic (seizure) □ Recovery Ix EEG for epilepsy ECG ± Holter monitor for arrhythmia Tilt-table test for neurogenic syncope and orthostatic hypotension Echocardiography for cardiomyopathy Blood glucose for hypoglycaemia - Page 77 of 179 - 4.1.2 Coma and Persistent Loss of Consciousness Ref: Davidson P. 1159, Neurology and Neurosurgery Illustrated P. 85, WCS29, 30 A. Physiology of Consciousness Consciousness: state of awareness of self and surrounding Components: □ Arousal: state of being ‘awake’ □ Awareness: cognitive and affective mental function (i.e. the ‘content’) Dependent on: □ Reticular activating system (RAS) in brainstem, hypothalamus, thalamus □ Cerebral hemisphere Reticular activating system (RAS): a loosely grouped aggregation of neurones in upper brainstem and medial thalamus □ Fx: maintains cerebral cortex in a state of wakeful consciousness □ Mechanism: → Thalamic relay neurones connected brainstem RAS neurones and activate cortical pyramidal neurones → govern level of consciousness → Tonic mode: thalamic neurones fire and activate cortex in a nonrhythmic (desynchronized manner) - Occurs in wakefulness or REM sleep → Burst mode: thalamic neurones fire55 and activate cortex in a rhythmic, bilateral synchronous manner → sleep spindles on EEG - Occurs in non-REM sleep B. Coma Coma: severe impairment of arousal ± awareness □ Definition: GCS ≤8 → No eye-opening to pain (E≤1) → Inability to speak (V≤2) → Inability to obey command (M≤5) □ Cause: suggestive of impairment of maintenance of arousal by RAS → Diffuse bilateral cortical impairment → Brainstem impairment (direct damage/suppression of RAS or its projections) 55 This is likely mediated by T-type Ca channels. - Page 78 of 179 - 1. Causes of Coma Intracranial lesions: □ Traumatic: diffuse white matter injury, haematoma □ Vascular: SAH, ICH, cerebral infarct with ↑ICP, brainstem infarct/haemorrhage □ Neoplastic: tumour with oedema □ Infective: meningitis, abscess, encephalitis □ Others: epilepsy, hydrocephalus Extracranial lesions: □ Metabolic: electrolyte imbalances, liver/renal failure, endocrine disorders □ Drugs/toxins: sedatives, anticonvulsants, anaesthetics, alcohol, heavy metals, CO… □ Vascular occlusion: vertebral artery disease, bilateral carotid disease □ Cardiorespiratory insufficiency □ Psychiatric: hysteria, catatonia 2. Approach to Coma Patients Cardiorespiratory stabilization GCS assessment Abort seizure if any (may ↑ICP) Control ICP if raised Investigate and treat underlying cause □ Hx and P/E as appropriate □ Blood test if extracranial diseases suspected → Should include L/RFT, BG, ABG, drug screen, blood culture (if pyrexic □ Urgent CT ± LP if intracranial diseases suspected 3. Terminology and Related Disorders of Consciousness Coma: deep sleep-like state from which patient cannot be aroused at all Stupor: state of baseline unresponsiveness with pt only aroused by vigorous stimuli Lethargy: state between alertness and stupod Vegetative state (VS): awake but unresponsive state □ No cognitive neurological function □ Retained non-cognitive (vegetative) neurological function (eg. cardiac action, respiration, maintenance of BP) □ May show head and limb movement but seldom meaningful response to external/internal environment □ Cause: extensive cortical gray/subcortical white matter lesion with relative preservation of brainstem functions → Most commonly cardiac arrest and head injuries □ Prognosis: almost nil in regaining mental fx after several months of PVS - Page 79 of 179 - Akinetic mutism: □ Partially or fully awake □ Able to form impressions and think but remains immobile and mute □ Cause: damage in medial thalamic nuclei, frontal lobe or hydrocephalus Abulia: mental and physical slowness with ↓ability to initiate activity □ Mild form of akinetic mutism Inattention: inability to sustain uninterrupted thought and actions □ Earliest outward sign: disorientation □ Can be an early sign of neurological disease (eg. encephalitis) Locked-in syndrome: □ Fully alert and aware with ability to carry out meaningful behaviour □ Completely paralyzed except for eye movements (quadriplegia + lower CN palsies) □ Cause: bilateral ventral pontine lesion (eg. basilar artery occlusion) Catatonia: hypomobile and mute syndrome a/w major psychosis □ Appear awake with eyes open □ Make no voluntary or responsive movements □ Blinks spontaneously, swallow and may not appear distressed □ NO clinical evidence of cerebral damage □ Long considered a psychiatric symptom but recently demonstrated in some neurological conditions (eg. NMDA receptor encephalitis) Pseudocoma (malingering) - Page 80 of 179 - 4.1.3 Delirium Ref: Davidson P. 1161, Crash Course in Psychiatry P. 106, WCS29 Delirium: acute confusional state with impairment in both consciousness and cognition □ Represents a common final pathway of disrupted homeostasis □ Very common (aka ‘decreased GC’), 14-24% among hospitalized, ↑ with age □ Heralds presence of life-threatening conditions in 10-30% older pt presenting to A&E (35-40% 1y mortality) Definition in DSM-V: Pathogenesis: poorly understood Clinical features: acute and fluctuating course of □ Impaired consciousness: ↓arousal, disorientation □ Inattention: ↓attention, concentration, ↑distractibility □ Disorganized thinking: disorganized or incoherent speech, rambling or irrelevant conversations □ Impaired cognition: disorientation, amnesia (recent > distant), language impairment, ↓comprehension □ Perceptual hallucination: illusions, hallucinations (30%) → Esp VH (psychotic ds more commonly presents with AH) □ Psychomotor disturbances: agitation or retardation □ Altered sleep-wake cycle: characteristic for delirium, ranges from daytime drowsiness + nighttime insomnia to complete sleep cycle reversal □ Mood disturbances: depression, euphoria, anxiety, anger, fear, apathy… Precipitating factors: □ Dementia: leading RF, 2/3 of delirium occurs in dementia patients □ ↓oral intake: dehydration, malnutrition □ Drugs: polypharmacy, psychotropics, alcohol abuse □ Medical conditions: severe illness, organ impairment, neurological disease, metabolic derangements, terminal illness Often confused with dementia: □ Both common in elderly □ Careful Hx taking