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234 Cards in this Set
- Front
- Back
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Transient Ischemic Stroke (TIA)
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Neurologic deficit that lasts from a few minutes to no more than 24 hours
Blockage of blood flow not long enough to cause permanent infarction *Distinguished from stroke by duration of symptoms |
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Risk of stroke after TIA
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30% 5 year risk
*TIAs are usually embolic |
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Most important general risk factors for stroke
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1) HTN
2) Age 3) Smoking 4) DM 5) AFib 6) CAD, Hyperlipidemia, previous stroke/TIA, carotid bruits, family hx |
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Stroke risk factors in younger patients
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1) OCPs
2) Hypercoagulable states (protein C or S deficiency, APLS) 3) Vasoconstrictive drug use (cocaine, amphetamines) 4) Polycythemia vera 5) Sickle cell disease |
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Locations of atherosclerotic lesions of thrombotic stroke
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1) Large neck arteries (carotid artery disease)
2) Medium-sized brain arteries (middle cerebral artery) |
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Origins of Embolic Strokes
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1) Heart (MC) - embolization of mural thrombus in pts with AFib
2) Internal carotid artery 3) Aorta 4) Paradoxical (Blood clots in peripheral veins pass through septal defects and reach the brain |
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Lacunar stroke
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Small vessel thrombotic disease
20% of strokes, often in subcortical structures (basal ganglia, thalamus, internal capsule, brainstem) *Narrowing of arterial lumen due to thickening of vessel wall; NOT THROMOSIS |
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MC risk factor for lacunar strokes
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HTN --> present in 80 - 90% of infarcts
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Arteries affected by lacunar infarcts
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1) Branches off of MCA
2) Arteries of Circle of Willis 3) Basilar and vertebral arteries |
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Clinical features of thrombotic stroke
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Neurological deficits with either rapid or stepwise onset
*Pt classically awakens with deficits |
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Transient Ischemic Stroke (TIA)
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Neurologic deficit that lasts from a few minutes to no more than 24 hours
Blockage of blood flow not long enough to cause permanent infarction *Distinguished from stroke by duration of symptoms |
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Risk of stroke after TIA
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30% 5 year risk
*TIAs are usually embolic |
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Most important general risk factors for stroke
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1) HTN
2) Age 3) Smoking 4) DM 5) AFib 6) CAD, Hyperlipidemia, previous stroke/TIA, carotid bruits, family hx |
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Stroke risk factors in younger patients
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1) OCPs
2) Hypercoagulable states (protein C or S deficiency, APLS) 3) Vasoconstrictive drug use (cocaine, amphetamines) 4) Polycythemia vera 5) Sickle cell disease |
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Locations of atherosclerotic lesions of thrombotic stroke
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1) Large neck arteries (carotid artery disease)
2) Medium-sized brain arteries (middle cerebral artery) |
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Origins of Embolic Strokes
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1) Heart (MC) - embolization of mural thrombus in pts with AFib
2) Internal carotid artery 3) Aorta 4) Paradoxical (Blood clots in peripheral veins pass through septa defects and reach the brain |
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Lacunar stroke
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Small vessel thrombotic disease
20% of strokes, often in subcortical structures (basal ganglia, thalamus, internal capsule, brainstem) *Narrowing of arterial lumen due to thickening of vessel wall; NOT THROMOSIS |
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MC risk factor for lacunar strokes
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HTN --> present in 80 - 90% of infarcts
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Arteries affected by lacunar infarcts
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1) Branches off of MCA
2) Arteries of Circle of Willis 3) Basilar and vertebral arteries |
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Clinical features of thrombotic stroke
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Neurological deficits with either rapid or stepwise onset
*Pt classically awakens with deficits |
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Transient Ischemic Stroke (TIA)
|
Neurologic deficit that lasts from a few minutes to no more than 24 hours
Blockage of blood flow not long enough to cause permanent infarction *Distinguished from stroke by duration of symptoms |
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Risk of stroke after TIA
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30% 5 year risk
*TIAs are usually embolic |
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Most important general risk factors for stroke
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1) HTN
2) Age 3) Smoking 4) DM 5) AFib 6) CAD, Hyperlipidemia, previous stroke/TIA, carotid bruits, family hx |
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Stroke risk factors in younger patients
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1) OCPs
2) Hypercoagulable states (protein C or S deficiency, APLS) 3) Vasoconstrictive drug use (cocaine, amphetamines) 4) Polycythemia vera 5) Sickle cell disease |
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Locations of atherosclerotic lesions of thrombotic stroke
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1) Large neck arteries (carotid artery disease)
2) Medium-sized brain arteries (middle cerebral artery) |
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Origins of Embolic Strokes
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1) Heart (MC) - embolization of mural thrombus in pts with AFib
2) Internal carotid artery 3) Aorta 4) Paradoxical (Blood clots in peripheral veins pass through septa defects and reach the brain |
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Lacunar stroke
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Small vessel thrombotic disease
20% of strokes, often in subcortical structures (basal ganglia, thalamus, internal capsule, brainstem) *Narrowing of arterial lumen due to thickening of vessel wall; NOT THROMOSIS |
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MC risk factor for lacunar strokes
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HTN --> present in 80 - 90% of infarcts
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Arteries affected by lacunar infarcts
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1) Branches off of MCA
2) Arteries of Circle of Willis 3) Basilar and vertebral arteries |
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Clinical features of thrombotic stroke
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Neurological deficits with either rapid or stepwise onset
*Pt classically awakens with deficits |
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Clinical features of embolic stroke
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Very rapid onset of neurological deficits
*MCA deficit: 1) Contralateral hemiparesis and hemisensory loss 2) Aphasia (dominant hemisphere) 3) Apraxia, contralateral body neglect (non-dominant hemisphere) |
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Clinical features of lacunar stroke
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Focal, contralateral PURE MOTOR or PURE SENSORY deficits
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Four major syndromes of lacunar stroke
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1) Pure motor - Internal capsule lesion
2) Pure sensory - Thalamic lesion 3) Ataxic hemiparesis - ipsilateral incoordination 4) Clumsy hand dysarthria |
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Diagnosis of stroke
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1) CT without contrast
2) MRI of brain 3) EKG 4) Carotid duplex 5) Magnetic Resonance Arteriogram (MRA) |
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CT imaging results after stroke
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Ischemic strokes appear dark
Hemorrhagic strokes appear white *May take 24 - 48 hours to see infarct but may exclude ICH |
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Complications of stroke
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1) Progression of neurologic insult
2) Cerebral edema may cause mass effects --> Mannitol lowers ICP 3) Hemorrhage into infarction (rare) 4) Seizures (>5% of pts) |
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Anterior Cerebral Artery stroke effects
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Contralateral lower extremity and face deficiency
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Middle Cerebral Artery stroke effects
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Aphasia
Contralateral hemiparesis |
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Vertebral/Basilar Artery stroke effects
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Ipsilateral: Ataxia, Diplopia, Dysphagia, Dysarthria, Vertigo
Contralateral: Homonymous Hemianopsia with basilar - PCA lesions Internal capsule: Pure motor hemiparesis Pons: Clumsy hand, dysarthria Thalamus: Pure sensory deficit |
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Treatment of stroke
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1) Thrombolytic therapy (t-PA) or aspirin
2) BP control 3) Prevention |
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Contraindications for t-PA
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1) More than 3 hours since ischemic stroke
2) Uncontrolled HTN 3) Bleeding disorder or anticoagulation 4) History of recent trauma or surgery |
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Role of heparin and warfarin in acute stroke
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Not proven to have efficacy --> generally not given in acute situation
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Indications for antihypertensive agents following stroke
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1) Systolic BP >220, diastolic >120, or MAP >130 mmHg
2) Significant medical indications for tx: Acute MI, aortic dissection, severe heart failure, hypertensive encephalopathy 3) Pt is receiving t-PA |
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Two major categories of hemorrhagic stroke
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1) Intracerebral hemorrhage (ICH) into parenchyma
2) Subarachnoid hemorrhage (SAH) into CSF |
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Causes of ICH
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1) HTN (sudden increase in BP causes rupture of small vessels deep within brain parenchyma)
2) Conversion from ischemic stroke 3) Amyloid angiopathy, anticoagulant use, brain tumors, AV malformations |
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Locations of ICH
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1) Basal ganglia (MC)
2) Pons 3) Cerebellum |
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Clinical features of ICH
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1) Abrupt onset of focal neurologic deficit (worsens steadily over 30 - 90 minutes)
2) AMS, stupor, coma 3) Headache, vomiting 4) Signs of increased intracranial pressure |
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Diagnosis of ICH
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Head CT diagnoses 95% of ICH
Coagulation panel and platelet count for bleeding diathesis |
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Complications of ICH
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1) Increased ICP
2) Seizures 3) Rebleeding 4) Vasospasm 5) Hydrocephalus 6) SIADH |
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Agent of choice to reduce BP after ICH
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Nitroprusside
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Stroke is associated with use of which illicit drug?
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Cocaine
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Given to reduce ICH after stroke
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Mannitol and diuretics
*Do not use prophylactically **DO NOT use steroids** |
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Pupillary findings in ICH
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Pons: Pinpoint pupils
Thalamus: Poorly reactive pupils Putamen: Dilated pupils |
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Common sites of SAH
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1) Junction of anterior communicating artery with anterior cerebral artery
2) Junction of posterior communicating artery with internal carotid artery 3) Bifurcation of MCA |
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Causes of SAH
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1) Ruptured Berry Aneurysm (MCC)
2) Trauma 3) AV malformation |
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Clinical features of SAH
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1) Sudden, excruciating headache w/o focal neurologic symptoms
2) Sudden, transient LOC 3) Vomiting 4) Meningeal irritation, nuchal rigidity, photophobia 5) Death 6) Retinal hemorrhage |
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Diagnosis of SAH
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1) CT scan w/o contrast
2) Lumbar puncture --> Blood in CSF is hallmark; Xanthochromia (yellow CSF due to RBC lysis) is gold standard *Cerebral angiogram detects site of bleeding for surgical clipping |
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Complications of SAH
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1) Rebleeding
2) Vasospasm 3) Hydrocephalus 4) Seizures 5) SIADH |
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Treatment of SAH
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1) Surgical - clipping of aneurysm
2) Medical - to reduce risk of rebleeding and vasospasm (Ca2+ channel blocker) |
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Contraindication to lumbar puncture
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Increased intracranial pressure
*Evidenced by papilledema |
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Characteristics of Parkinson's Disease
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1) Loss of dopamine-containing neurons in pars compacta of substantia nigra (& locus ceruleus)
2) Essentially a clinical diagnosis |
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Clinical features of Parkinson's Disease
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1) Resting tremor (pill-rolling)
2) Bradykinesia - slowing of voluntary movements 3) Cogwheel rigidity - ratchet-like jerking 4) Poor postural reflexes --> shuffling gait, stooped posture 5) Masked facies - decreased blinking 6) Depression, dementia |
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Shy-Drager Syndrome
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Parkinsonian symptoms plus autonomic insufficiency
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Medications associated with Parkinsonism
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1) Neuroleptics
2) Metoclopramide 3) Reserpine |
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Treatment of Parkinson's Disease
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1) Carbidopa-Levodopa (Sinemet)
2) Dopamine-receptor agonists (Pergolide, Bromocriptine, Pramipexole) 3) Selegiline (MAOI) 4) Amantidine 5) Anticholinergics (Trihexyphenidyl, Benztropine) 6) Amitriptyline 7) Surgery (deep brain stimulation) |
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Side effects of Carbidopa-Levodopa
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1) Dyskinesias (involuntary, choreic movements) --> reason for delayed tx
2) Levodopa has on-off fluctuations |
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Difference between Progressive Supranuclear Palsy (PSP) and Parkinson's
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PSP does not cause tremor, but does cause ophthalmoplegia
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Huntington's Chorea
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Autosomal dominant mutation on chromosome 4
Expanded CAG repeats cause loss of GABA-producing neurons in STRIATUM |
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Clinical features of Huntington's Chorea
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1) Chorea - face, head, neck, tongue, trunk, extremities
2) Altered behavior - irritability, personality changes, depression 3) Progressive dementia 4) Unsteady and irregular gait 5) Incontinence |
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Diagnosis of Huntington's Chorea
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1) MRI - atrophy of caudate nuclei
2) DNA testing |
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Treatment of Huntington's Chorea
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1) Dopamine blockers help psychosis and chorea
2) Anxiolytics 3) Antidepressants *There is no cure |
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3 Types of Tremor
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1) Physiologic
2) Essential 3) Neurologic disease |
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Causes of Physiologic Tremor
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1) Fear, anxiety, fatigue
2) Metabolic - HYPOglycemia, HYPERthyroidism, Pheochromocytoma 3) Toxic - EtOH withdrawl, valproic acid, lithium, caffeine, theophylline) |
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Treatment of Physiologic Tremor
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Treat underlying cause
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Essential Tremor
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Autosomal dominant (33%)
Induced by intentional activity; Decreased with EtOH use Treated with Propranolol |
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Characteristics of Ataxia
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1) Gait instability
2) Loss of balance 3) Impaired limb coordination |
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Causes of Ataxia
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1) Acquired - EtOH, vitamin B12 or thamine deficiency, cerebellar infarct, neoplasm, demyelinating disease, tabes dorsalis
2) Inherited - Friedreich's ataxia, Ataxia Telangiectasia |
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Friedreich's Ataxia
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Autosomal recessive - onset in young adulthood
Ataxia, nystagmus, impaired vibration and proprioception |
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Ataxia Telangectasia
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Autosomal recessive - childhood onset
Ataxia, nystagmus, impaired vibration and proprioception, telangectasias *Increased incidence of cancer |
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Treatment of Ataxia
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Treat underlying cause if possible
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Psychiatric diagnosis associated with Tourette's Syndrome
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Obsessive-Complusive Disorder
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Clinical features of Tourette's
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1) Motor tics
2) Vocal tics |
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Treatment of Tourette's Syndrome
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1) Pimozide
2) Clonidine 3) Haloperidol |
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Dementia
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Progressive deterioration of intellectual function with preservation of consciousness
*Most important risk factor is age |
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Differential diagnosis of Dementia
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1) Primary neurologic disorder
2) Infection 3) Metabolic disorder 4) Drugs and toxins 5) Pseudodementia (depression) |
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Neurologic causes of dementia
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1) Alzheimer's Disease
2) Vascular dementia 3) Space-occupying lesions 4) Normal pressure hydrocephalus 5) Lewy-body dementia 6) Pick's disease 7) MS, Parkinson's, Huntington's, Wilson's Disease |
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Multi-infarct Dementia
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Stepwise intellectual decline due to series of cerebral infarctions
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Binswanger's Disease
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Insidious onset of intellectual decline due to diffuse subcortical white matter degeneration
*Associated with long-standing HTN and atherosclerosis |
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Infectious causes of dementia
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1) HIV (AIDS-related dementia)
2) Neurosyphilis 3) Cryptococcal infection 4) Creutzfeldt-Jakob disease 5) Progressive multifocal leukoencephalopathy |
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Metabolic causes of dementia
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1) Thyroid disease (HYPO or HYPER)
2) Vitamin B12 deficiency 3) Thiamine deficiency (alcoholics) 4) Niacin deficiency |
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Laboratory studies to investigate cause of dementia
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1) CBC with differential
2) CMP 3) TSH, T4 4) Vitamin B12, folate 5) VDRL 6) HIV 7) CT or MRI |
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Medical therapy for dementia
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1) Vitamin E
2) Tacrine 3) Donepezil *Evidence supporting these tx is inconclusive |
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Risk Factors for Alzheimer's Disease
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1) Family hx
2) Down's Syndrome |
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Pathologic findings in Alzheimer's
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1) Senile plaques - focal collections of dilated, tortuous neuritic processes surrounding central amyloid beta-protein
2) Neurofibrillary tangles - bundles of neurofilaments in nuclear cytoplasm |
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Early stage of Alzheimer's
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Mild forgetfulness, impaired ability to learn new material, poor concentration, personality changes
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Intermediate stage of Alzheimer's
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Progressive memory impairment, visuospatial disturbances, verbal repetition
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Late stage of Alzheimer's
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Assistance needed for ADL, difficulty remembering names of family members, paranoid delusions and hallucinations
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Imaging in Alzheimer's
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Diffuse cortical atrophy with ventricle enlargement
*Clinical diagnosis |
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Treatment of Alzheimer's
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1) AChE inhibitors - 1st line agent
2) Tacrine (QID) *Vitamin E had benefit in one study |
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Delirium
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Acute period of cognitive dysfunction due to medical disturbance or condition
Elderly pts especially prone |
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Causes of delirium
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1) Postoperative state
2) Dehydration, drug intoxication 3) Infection, inflammation, fever 4) Medications, malnutrition, metals 5) Withdrawal states (EtOH, benzos) 6) Trauma, burns |
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Diagnosis of delirium
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1) Mental status exam
2) Labs 3) LP - performed in any febrile, delirious pt |
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Treatment of delirium
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1) Treat underlying cause
2) Haloperidol for agitation |
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Necessary for arousal and cognition
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Arousal: Intact brainstem
Cognition: Intact cerebral cortex |
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Coma
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Depressed level of consciousness such that pt is completely unresponsive to stimuli
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Causes of coma
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1) Structural brain lesions (usually bilateral)
2) Global brain dysfunction (metabolic or systemic disorders) 3) Psychiatric causes (conversion disorder) |
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Differential diagnosis of coma
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S- Structural brain pathology
M- Meningitis, mental illness A- Alcohol, acidosis S- Seizures H- Hypercapnia, hyperglycemia, hyponatremia, hypoxia E- Endocrine, encephalitis, electrolytes D- Drugs |
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Pupillary status associated with Uncal herniation
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Anisocoria - asymmetric pupils
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Pupillary status in severe anoxia
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Bilateral, fixed, dilated pupils
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Pupillary status with CN III compression
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Unilateral, fixed, dilated pupil
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Pupillary status with narcotic use or ICH
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Pinpoint pupils
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Oculocephalic test with intact brainstem
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When head is turned to one side, eyes should move conjugately to the opposite side
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Labs to do in pt in coma
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CBC, electrolytes, Ca2+, BUN, ABGs, glucose, creatinine, EKG, toxicology
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"Locked In" Syndrome
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Pts completely paralyzed with sparing of muscles for respiration, blinking, and vertical eye movement
Pts fully aware of surroundings and capable of feeling pain *Due to infarction or hemorrhage of Ventral Pons* |
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Sites of Brain Herniation
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1) Uncal (transtentorial) herniation
2) Tonsillar herniation 3) Central herniation |
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Uncal Herniation
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Uncus compresses MIDBRAIN
Compression of CN III --> Ipsilateral anisocoria, dilated pupil, sluggish pupillary reflex Contralateral hemiparesis (compression of cerebral peduncle) Can lead to death via cardiopulmonary compromise |
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Tonsillar Herniation
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Medial portions of cerebellar hemispheres compress MEDULLA through foramen magnum
Compression of cardiopulmonary center can cause rapid death |
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Central Herniation
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Supratentorial lesions
Cheyne-Stokes respirations, hyperventilation, extremity posturing, increased muscle tone, bilateral Babinski sign |
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Treatment of Brain Herniation
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1) Intubation
2) Neurosurgery consult 3) Lower ICP |
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Multiple Sclerosis
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Demyelination of CNS white matter and spinal cord
*Classically at angles of lateral ventricles |
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Tracts commonly affected by Multiple Sclerosis (MS)
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1) Pyramidal and cerebellar pathways
2) Medial longitudinal fasciculus 3) Optic nerve 4) Posterior columns |
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Clinical features of MS
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1) Transient sensory deficits
2) Fatigue 3) Motor weakness or spasticity (pyramidal tract involvement) 4) Visual disturbances: Optic neuritis, Internuclear ophthalmoplegia 5) Cerebellar involvement --> ataxia, dysarthria, intention tremor 6) Neuropathic pain - hyperesthesias and trigeminal neuralgia |
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Optic Neuritis
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Monocular vision loss
Pain on eye movement Central scotoma (black spot) Decreased pupillary reaction to light |
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Internuclear Ophthalmoplegia
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Lesion in medial longitudinal Fasiculus
Ipsilateral medial rectus palsy on attempted lateral gaze and horizontal nystagmus *Affected eye cannot adduct |
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Diagnostic test of choice for MS
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MRI
*On LP, OLIGOCLONAL BANDS of IgG present in 90% of MS patients |
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Treatment of acute attacks of MS
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1) High-dose IV corticosteroids shorten attack
2) Interferon therapy 3) Baclofen for muscle spasticity 4) Carbamazepine or Gabapentin for neuropathic pain *Cyclophosphamide reserved for rapidly progressive disease due to SEs |
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Gullian-Barre Syndrome
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INFLAMMATORY demyelinating polyneuropathy primarily affecting motor nerves
Preceded by viral or mycoplasmal infection of upper respiratory or GI tract *Also seen in Hodgkin's disease, SLE, post-surgery, or HIV seroconversion |
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Clinical features of Gullian-Barre Syndrome
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1) Abrupt onset of rapidly progressive ascending paralysis of all 4 extremities
2) Autonomic features - arrhytmias, tachycardia, postural hypotension *Can cause respiratory failure *Sensory, sphincter tone, and mentation usually intact |
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Diagnosis of Gullian-Barre Syndrome
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1) CSF - elevated protein, normal cell count
2) Electrodiagnostic studies - decreased motor nerve conduction velocity |
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Treatment of Gullian-Barre Syndrome
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1) Monitor pulmonary function --> mechanical ventilation if necessary
2) IV Ig for significant weakness 3) Plasmaphersis may reduce disease severity **DO NOT give STEROIDS --> They are harmful** |
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MC intracranial neoplasm in adults
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Brain Metastasis
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MC primary CNS tumors in adults
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1) Gliomas
2) Meningiomas |
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Clinical features of CNS Neoplasms
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1) Headache
2) Nausea / vomiting 3) Reduced level of consciousness 4) Papilledema 5) Brain herniation (rapidly growing tumor) 6) Focal deficits (CNs, seizures, visual disturbances, aphasia, etc) |
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Diagnosis of CNS Neoplasms
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1) MRI with and without Gadolinium
2) Brain biopsy |
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Two important indications for MRI to rule out intracranial mass
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1) New-onset seizure in adult
2) New and persistent or progressive headache |
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CNS tumors with good prognosis after resection
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1) Meningioma
2) Schwannoma 3) Pituitary adenoma |
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CNS tumors unable to be resected
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Gliomas (astrocytomas, oligodendrogliomas)
*Radiation may prolong survival |
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Astrocytomas
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MC primary CNS neoplasm
Arise in cerebral hemispheres Tend to cross corpus callosum into opposite hemisphere Poor prognosis *Glioblastoma Multiforme has worst prognosis* |
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Oligodendrogliomas
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Peak occurrence between 40 - 50 years old
Malignant, but more indolent than fibrillary astrocytomas *Survival: 10 - 15 years |
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Primary CNS Lymphoma
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Related to immunosuppression
AIDS patients and transplant recipients highly susceptible *5-year survival less than 5% |
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MC primary neoplasms that metastasize to the brain
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1) Lung
2) Breast 3) Skin 4) Kidney 5) GI tract |
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Meningiomas
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Extracerebral, well-defined round masses attached to the dura and compressing underlying brain
*Potential for surgical cure, but high recurrence |
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Schwannomas
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Benign tumors (no malignant potential)
Bilateral --> pathognomonic for Neurofibromatosis Type II Arise in cerebellopontine angle --> involves CN8 --> Hearing loss Surgical resection achieves cure |
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Differential Diagnosis of Ring-Enhancing Brain Lesion
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1) Metastatic CA
2) Brain Abscess 3) Glioblastoma Multiforme 4) Lymphoma 5) Toxoplasmosis |
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Meningeal Carcinomatosis
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CA metastasis to meninges --> Focal deficits
CSF reveals malignant cells, elevated protein and lymphocytes and decreased glucose *Treat with intrathecal chemotherapy |
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Secondary insults of Head Trauma
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1) Hypotension --> cerebral hypoperfusion
2) Hypoxia --> brainstem compression leads to apnea 3) Hypercapnia --> causes vasodilation and increases intravascular volume 4) Increased ICP 5) Intracranial mass effect 6) Anemia - blood loss |
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Most common cause of death after severe head injury
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Increased intracranial pressure
*Normal ICP is 5-10mm H2O *ICP > 20mm is worrisome **Bilateral fixed and dilated pupils suggest diffusely increased ICP** |
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Signs of basilar skull fracture
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1) Raccoon eyes
2) Battle sign 3) Otorhhea or CSF rhinorrhea 4) Hemotympanum |
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Cerebral Perfusion Pressure (equation)
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Mean arterial pressure minus intracranial pressure
*Normal CPP is >50mm Hg |
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Key features of Head Trauma
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1) Increased ICP
2) Epidural or Subdural hematoma 3) Herniation 4) Signs of basilar fracture 5) Coup or contrecoup injury 6) Seizures 7) Diffuse axonal injury |
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Cushing's Triad
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Physiologic response to increased ICP
1) Hypertension 2) Bradycardia 3) Respiratory irregularity *If present, ICP is life-threatening |
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General techniques to lower ICP
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1) Reverse Trendelenburg position
2) Intubation with hyperventilation 3) Mannitol 4) Lowering body temperature slightly 5) Draining CSF if ventricular catheter in place |
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Epidural Hematoma
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Blood clot between skull and dura
Typically due to laceration of middle meningeal artery with temporal bone fracture |
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Clinical features of epidural hematoma
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1) Brief LOC followed by lucid interval
2) Coma occurs as hematoma enlarges and compresses midbrain 3) Ipsilateral blown pupil (seen in 50% of cases) *CT shows (bi)convex mass overlaying the brain *Treat with rapid surgical decompression |
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Subdural Hematoma
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Blood clot between dura and the brain
Results from venous bleeding after blunt head trauma *CT scan shows concave mass (crescent-shaped) |
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Risk factors for subdural hematoma
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1) Brain atrophy (alcoholics and elderly patients)
2) Anticoagulated patients |
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Clinical features of acute subdural hematoma
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Mass effect --> decline in mental status and change in level of consciousness
Poor prognosis *Prompt surgical evacuation indicated |
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Clinical features of chronic subdural hematoma
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Symptoms occur at least 1 week after injury
No loss of consciousness May resolve if small |
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Typical findings with subdural hematomas
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1) Decreased level of consciousness
2) Headache 3) Cortical dysfunction |
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Concussion
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Brain injury related to blunt trauma that results in brief LOC
Caused by electrophysiologic dysfunction of the midbrain 2/2 impact Confusion, dizziness, difficulty concentrating may be present *Vomiting delirium, and focal neurologic deficits suggest elevated ICP |
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Myasthenia Gravis
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Autoimmune disorder --> antibodies against nicotinic ACh receptors at neuromuscular junction
Reduced postsynaptic response and significant muscle fatigue |
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Clinical features of Myasthenia Gravis
|
1) Skeletal muscle weakness (extraocular muscles, eyelids, facial muscles, proximal limbs)
2) Ptosis, diplopia, blurred vision (MC initial symptoms) 3) Generalized weakness, dysarthria, dysphagia 4) Slow progression with periodic exacerbations *Myasthenic crisis - medical emergency occurring in 15% of patients (diaphragmatic fatigue) |
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Diagnosis of Myasthenia Gravis
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1) Edrophonium (Tensilon) test - AChE medication causes marked improvement of symptoms
2) ACh receptor antibody test 3) EMG - decremental response to repetitive motor neuron stimulation *CT scan of thorax can rule out thymoma |
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Treatment of Myasthenia Gravis
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1) AChE inhibitors - Pyridostigmine
2) THYMECTOMY 3) Immunosuppressive drugs (corticosteroids first) 4) Plasmapheresis removes antibodies 5) IVIG 6) Intubation if necessary |
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Medications that exacerbate Myasthenia Gravis symptoms
|
1) Aminoglycosides and tetracyclines
2) Beta-blockers 3) Anti-arrhythmics (Quinidine, Procainamide, Lidocaine) |
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Lambert-Eaton Syndrome
|
**Associated with Small Cell Lung Cancer**
Autoantibodies against PREsynpatic CALCIUM channels Proximal muscle weakness and HYPOreflexia *Symptoms improve with increased muscle stimulation* |
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Duchenne's Muscular Dystrophy
|
X-lined recessive mutation in Dystophin gene
*No inflammation* |
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Clinical features of Duchenne's Muscular Dystrophy
|
1) Progressive, symmetric, proximal muscle weakness that begins in childhood
2) Gower's maneuver (hands used when rising from floor) 3) Pseudohypertrophy of calf muscles 4) Wheelchair confinement, respiratory failure, and death in 3rd decade |
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Diagnosis of Duchenne's Muscular Dystrophy
|
1) Serum creatinine phosphokinase levels
2) DNA testing |
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Treatment of Duchenne's Muscular Dystrophy
|
No treatment available
Predisone may slow progression Surgery may correct scoliosis |
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Becker's Muscular Dystrophy
|
X-linked recessive mutation in Dystophin gene, but less severe than Duchenne's --> some dystrophin present
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Neurofibromatosis Type I (von Recklinghausen's Disease)
|
Autosomal dominant disorder
Cafe au lait spots, neurofibromas, CNS tumors, axillary freckling, iris hamartomas (Lisch nodules), bony lesions |
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CNS tumors associated with NF1
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1) Gliomas
2) Meningiomas |
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Complications of NF1
|
1) Scoliosis
2) Pheochromocytomas 3) Optic nerve gliomas 4) Renal artery stenosis 5) Erosive bone defects (spinal deformity, congenital tibial dysplasia) |
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Neurofibromatosis Type II
|
Autosomal dominant disorder
Bilateral acoustic neuromas (schwannomas), multiple meningiomas, neurofibromas, cataracts |
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Other features of Neurofibromatosis
|
1) Seizures
2) Mental retardation, learning disabilities 3) Short height 4) Macrocephaly |
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Tuberous Sclerosis
|
Autosomal dominant
Skin lesions (facial angiofibromas, adenoma sebaceum) Cognitive impairment, epilepsy, retinal hamartomas, renal angiomyolipomas, cardiac rhabdomyomas |
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Sturge-Weber Syndrome
|
Acquired disorder
Capillary angiomatoses of pia mater *Port-wine stain* *Epilepsy and mental retardation* Treatment of epilepsy is mainstay of treatment |
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Von Hippel-Lindau Disease
|
Autosomal Dominant
CAVERNOUS HEMANGIOMAS of brain or brainstem, renal angiomas, cysts in multiple organs *Associated with Renal Cell Carcinoma* |
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Syringomyelia
|
Central cavitation of CERVICAL spinal cord --> abnormal fluid collection w/in cord parenchyma
*Diagnosed by MRI *Treated by surgical syringosubarachnoid shunt |
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Causes of syringomyelia
|
1) Cranial base malformation (Arnold-Chiari malformation)
2) Intramedullary tumors 3) Traumatic necrosis of cord |
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Clinical features of Syringomyelia
|
Bilateral loss of PAIN & TEMPERATURE over shoulders (capelike distribution) --> Lateral Spinothalamic Tract
*Muscle atrophy of hands may occur |
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Brown-Sequard Syndrome
|
Spinal cord hemisection resulting in
CONTRAlateral loss of pain and temp (Spinothalamic tract) and IPSIlateral hemiparesis (Corticospinal tract), and IPSIlateral loss of position/vibration (Dorsal columns) |
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Transverse Myelitis
|
Rare condition affecting horizontal aspects of spinal cord (idiopathic)
Lower extremity weakness, back pain, sensory deficits below lesion, sphincter disturbance *High-dose steroid therapy equivocal |
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Horner's Syndrome
|
1) Miosis
2) Anhydrosis 3) Ptosis *Interruption of cervical sympathetic nerves |
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Causes of Horner's Syndrome
|
1) Idiopathic
2) Pancoast tumor (pulmonary apex) 3) Internal carotid dissection 4) Brainstem stroke 5) Neck trauma (cervical spine injury) |
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Poliomyelitis
|
Poliovirus damage to anterior horn cells and motor neurons of spinal cord and brainstem --> LMN signs
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Clinical features of Polio
|
1) Asymmetric muscle weakness (legs)
2) Absent deep tendon reflexes 3) Flaccid, atrophic muscles 4) NORMAL sensation (dorsal columns uninvolved) *Bulbar involvement (CN IX, X) can lead to respiratory and cardio impairment *No treatment, but prevented by vaccination |
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3 major causes of Dizziness
|
1) Presyncope (lightheadedness)
2) Vertigo 3) Multisensory stimuli (sensory overload) |
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Vertigo
|
Disturbance of vestibular system --> sensation of spinning or hallucination of movement
Peripheral (benign) or central |
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Causes of Peripheral Vertigo
|
1) Meniere's Disease
2) Benign positional vertigo 3) Acute labyrinthitis - due to viral infection of cochlea and labyrinth 4) Ototoxic drugs (aminoglycosides, some diuretics) 5) Acoustic neuroma |
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Meniere's Disease
|
Triad of
1) Vertigo 2) Tinnitis 3) Hearing loss *Attacks wax and wane; hearing loss eventually becomes permanent |
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Benign Positional Vertigo
|
Vertigo only in specific positions or during change in position
Abrupt onset Usually in patients >60, and after head injury Recovery usually complete (resolves within 6 months) |
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Causes of Central Vertigo
|
1) Multiple Sclerosis
2) Vertebrobasilar insufficiency 3) Migraine-associated vertigo (w/ or w/o headache) |
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Syncope
|
Transient loss of consciousness/postural tone 2/2 acute decrease in cerebral blood flow
Rapid recovery of consciousness w/o resuscitation |
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Causes of syncope
|
1) Seizure disorder
2) Cardiac causes 3) Vasovagal causes 4) Orthostatic hypotension 5) Severe cerebrovascular disease 6) Others (metabolic, hypersensitivity, decreased venous return, etc) |
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Cardiac Syncope
|
Usually sudden, without prodromal symptoms
Caused by 1) Arrhythmias 2) Obstruction of blood flow (aortic stenosis, hypertrophic cardiomyopathy, pulmonary HTN, atrial myxoma, etc) 3) Massive MI |
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Vasovagal Syncope
|
MCC of syncope
Precipitated by emotion, pain, fear, claustrophobic situations Tilt-table study reproduces symptoms |
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Medical treatment of vasovagal syncope
|
1) Beta-blockers
2) Disopyramide |
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Treatment of Orthostatic Syncope
|
1) Increased salt intake and fluids
2) Fludrocortisone |
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|
Main goal in the diagnosis of syncope
|
Differentiate between cardiac and non-cardiac etiologies
*Ask events before, during, and after episode, as well as medications |
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Physical exam in evaluation of syncope
|
1) Orthostatic BPs and pulse
2) Mental status (post-ictal state) 3) Murmurs 4) Carotid pulses |
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Diagnostic tests for Syncope
|
1) EKG (ALL patients)
2) CBC, CMP 3) Holter monitoring 4) CT scan or EEG 5) Echocardiogram 6) Tilt-table testing |
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Seizure
|
Sudden abnormal discharge of electrical activity in the brain
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Causes of Seizure (4 Ms, 4 Is)
|
M-Metabolic and electrolytes
M-Mass lesions M-Missing drugs (anticonvulsant noncompliance, EtOH or benzo withdrawal) M-Miscellaneous (pseudoseizures, pre-eclampsia) I-Intoxications (cocaine, lithium, lidocaine, metals, etc) I-Infections I-Ischemia I-Increased ICP |
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|
Metabolic causes of seizure
|
1) HYPOnatremia
2) HYPOcalcemia 3) HYPO or HYPERglycemia 4) HYPERthermia 5) Uremia 6) Thyroid storm 7) Water intoxication |
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|
Simple Partial Seizure
|
*Consciousness remains intact*
Localized, but may evolve to be complex *May involve transient, unilateral clonic-tonic movement |
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|
Complex Partial Seizure
|
*Consciousness is impaired; Post-ictal confusion*
Automatisms - purposeless, involuntary repetitive movements Olfactory or gustatory hallucinations |
|
|
Generalized seizure
|
*LOC*
Tonic-clonic (grand mal) or absence (petit mal) |
|
|
Tonic clonic seizure
|
Bilaterally symmetric without focal onset
Begins with LOC and fall to the ground Tonic phase - rigidity, trunk and limb extension Clonic phase - musculature jerking for at least 30 seconds Patient becomes flaccid and comatose before regaining consciousness Post-ictal confusion Tongue biting, vomiting, apnea, incontinence |
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Absence seizure
|
School-aged children stare into space then return to activity several seconds later
Minor clonic activity (eye blinking or head nodding) Episodes are brief but may be frequent *No loss of postural tone or continence, no post-ictal confusion* |
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|
Diagnostics test for Seizure
|
1) CBC, electrolytes, glucose, LFTs, renal function tests, serum Ca2+, urinalysis
2) EEG 3) CT scan 4) MRI - brain 5) LP and blood cultures if pt is febrile |
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|
Anticonvulsant agents for generalized tonic-clonic and partial seizures
|
Phenytoin and Carbamazepine are drugs of choice
*Other options: phenobarbital, valproate, primidone |
|
|
Anticonvulsant agents for absence seizures
|
Ethosuximide and Valproic Acid
|
|
|
Status Epilepticus
|
Prolonged, sustained unconsciousness with persistent convulsive activity in a seizing patient
*Medical emergency *Manage with IV diazepam, phenytoin, and 50mg dextrose --> resistant cases treated with IV phenobarbital |
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|
Amyotrophic Lateral Sclerosis (ALS)
|
Disorder affecting anterior horn cells and corticospinal tracts at many levels (corticobulbar tract as well)
*Presence of UMN and LMN signs is hallmark Onset between 50 - 70 Dismal prognosis |
|
|
Clinical features of ALS
|
1) Progressive muscle weakness
2) Muscle cramps and spasticity 3) Fasciculations 4) Impaired speech and swallowing 5) Respiratory muscle weakness 6) Weight loss and fatigue 7) Normal continence, sensation, cognition, and EOM |
|
|
Diagnosis of ALS
|
1) EMG and nerve conduction studies - confirms degeneration of LMNs and r/o NMJ disorders
2) Clinical evidence: 2 or more regions involved |
|
|
Treatment of ALS
|
Supportive
Riluzole, glutamate-blocking agent, may delay death by 3-5 months |
|
|
Aphasia
|
The loss or defect of language (speaking, fluency, reading, writing, comprehension, etc)
|
|
|
4 Types of Aphasia
|
1) Wernicke's
2) Broca's 3) Conduction 4) Global |
|
|
Causes of Aphasia
|
1) Stroke (MCC)
2) Brain trauma 3) Brain tumor 4) Alzheimer's Disease |
|
|
Wernicke's Aphasia
|
Receptive, fluent aphasia
*Impaired comprehension of written or spoken language* Speech is grammatically correct and fluid, but makes no sense --> Patients don't understand their own words |
|
|
Broca's Aphasia
|
Expressive, nonfluent aphasia
Speech is slow and requires effort Pt uses short sentences without grammatical construction Good comprehension of written and spoken language *Often associated with right hemiparesis and hemisensory loss |
|
|
Conduction Aphasia
|
Disturbance in repetition
Pathology involving connections between Wernicke's and Broca's areas |
|
|
Global Aphasia
|
Disturbance in all areas of language function
*Often associated with right hemiparesis |
|
|
Treatment of Aphasia
|
Most patients recover spontaneously
Speech therapy |
|
|
Bell's Palsy
|
Hemifacial weakness/paralysis of muscles innervated by CN VII
Due to swelling of CN *Good prognosis - 80% recover spontaneously |
|
|
Causes of Bell's Palsy
|
1) Idiopathic
2) Possible viral etiology (herpes simplex) 3) URI common preceding event |
|
|
Treatment of Bell's Palsy
|
1) Usually, none
2) Prednisone and Acyclovir if necessary 3) Eye patch at night to prevent corneal abrasion 4) Surgical decompression of CN VII if paralysis progresses |
|
|
Trigeminal Neuralgia (Tic Douloureux)
|
Brief (seconds to minutes) but frequent attacks of severe, lancinating facial pain
Involves jaw, lips, gums, maxillary area Recurrent attacks *One of the most painful conditions known |
|
|
Why does one get an MRI in diagnosis of Tic Douloreux?
|
To rule out cerebellopontine angle tumor
|
|
|
Treatment of Trigeminal Neuralgia
|
1) Carbamazepine (DOC)
2) Baclofen 3) Phenytoin 4) Surgical decompression |
|
|
Differential Diagnosis of Facial Nerve Palsy
|
1) Trauma
2) Lyme disease 3) Tumor 4) Guillain-Barre Syndrome 5) Herpes Zoster |
