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234 Cards in this Set

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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
Risk of stroke after TIA
30% 5 year risk

*TIAs are usually embolic
Most important general risk factors for stroke
1) HTN
2) Age
3) Smoking
4) DM
5) AFib
6) CAD, Hyperlipidemia, previous stroke/TIA, carotid bruits, family hx
Stroke risk factors in younger patients
1) OCPs
2) Hypercoagulable states (protein C or S deficiency, APLS)
3) Vasoconstrictive drug use (cocaine, amphetamines)
4) Polycythemia vera
5) Sickle cell disease
Locations of atherosclerotic lesions of thrombotic stroke
1) Large neck arteries (carotid artery disease)
2) Medium-sized brain arteries (middle cerebral artery)
Origins of Embolic Strokes
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
Lacunar stroke
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
MC risk factor for lacunar strokes
HTN --> present in 80 - 90% of infarcts
Arteries affected by lacunar infarcts
1) Branches off of MCA
2) Arteries of Circle of Willis
3) Basilar and vertebral arteries
Clinical features of thrombotic stroke
Neurological deficits with either rapid or stepwise onset

*Pt classically awakens with deficits
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
Risk of stroke after TIA
30% 5 year risk

*TIAs are usually embolic
Most important general risk factors for stroke
1) HTN
2) Age
3) Smoking
4) DM
5) AFib
6) CAD, Hyperlipidemia, previous stroke/TIA, carotid bruits, family hx
Stroke risk factors in younger patients
1) OCPs
2) Hypercoagulable states (protein C or S deficiency, APLS)
3) Vasoconstrictive drug use (cocaine, amphetamines)
4) Polycythemia vera
5) Sickle cell disease
Locations of atherosclerotic lesions of thrombotic stroke
1) Large neck arteries (carotid artery disease)
2) Medium-sized brain arteries (middle cerebral artery)
Origins of Embolic Strokes
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
Lacunar stroke
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
MC risk factor for lacunar strokes
HTN --> present in 80 - 90% of infarcts
Arteries affected by lacunar infarcts
1) Branches off of MCA
2) Arteries of Circle of Willis
3) Basilar and vertebral arteries
Clinical features of thrombotic stroke
Neurological deficits with either rapid or stepwise onset

*Pt classically awakens with deficits
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
Risk of stroke after TIA
30% 5 year risk

*TIAs are usually embolic
Most important general risk factors for stroke
1) HTN
2) Age
3) Smoking
4) DM
5) AFib
6) CAD, Hyperlipidemia, previous stroke/TIA, carotid bruits, family hx
Stroke risk factors in younger patients
1) OCPs
2) Hypercoagulable states (protein C or S deficiency, APLS)
3) Vasoconstrictive drug use (cocaine, amphetamines)
4) Polycythemia vera
5) Sickle cell disease
Locations of atherosclerotic lesions of thrombotic stroke
1) Large neck arteries (carotid artery disease)
2) Medium-sized brain arteries (middle cerebral artery)
Origins of Embolic Strokes
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
Lacunar stroke
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
MC risk factor for lacunar strokes
HTN --> present in 80 - 90% of infarcts
Arteries affected by lacunar infarcts
1) Branches off of MCA
2) Arteries of Circle of Willis
3) Basilar and vertebral arteries
Clinical features of thrombotic stroke
Neurological deficits with either rapid or stepwise onset

*Pt classically awakens with deficits
Clinical features of embolic stroke
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)
Clinical features of lacunar stroke
Focal, contralateral PURE MOTOR or PURE SENSORY deficits
Four major syndromes of lacunar stroke
1) Pure motor - Internal capsule lesion
2) Pure sensory - Thalamic lesion
3) Ataxic hemiparesis - ipsilateral incoordination
4) Clumsy hand dysarthria
Diagnosis of stroke
1) CT without contrast
2) MRI of brain
3) EKG
4) Carotid duplex
5) Magnetic Resonance Arteriogram (MRA)
CT imaging results after stroke
Ischemic strokes appear dark
Hemorrhagic strokes appear white

*May take 24 - 48 hours to see infarct but may exclude ICH
Complications of stroke
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)
Anterior Cerebral Artery stroke effects
Contralateral lower extremity and face deficiency
Middle Cerebral Artery stroke effects
Aphasia
Contralateral hemiparesis
Vertebral/Basilar Artery stroke effects
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
Treatment of stroke
1) Thrombolytic therapy (t-PA) or aspirin
2) BP control
3) Prevention
Contraindications for t-PA
1) More than 3 hours since ischemic stroke
2) Uncontrolled HTN
3) Bleeding disorder or anticoagulation
4) History of recent trauma or surgery
Role of heparin and warfarin in acute stroke
Not proven to have efficacy --> generally not given in acute situation
Indications for antihypertensive agents following stroke
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
Two major categories of hemorrhagic stroke
1) Intracerebral hemorrhage (ICH) into parenchyma
2) Subarachnoid hemorrhage (SAH) into CSF
Causes of ICH
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
Locations of ICH
1) Basal ganglia (MC)
2) Pons
3) Cerebellum
Clinical features of ICH
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
Diagnosis of ICH
Head CT diagnoses 95% of ICH
Coagulation panel and platelet count for bleeding diathesis
Complications of ICH
1) Increased ICP
2) Seizures
3) Rebleeding
4) Vasospasm
5) Hydrocephalus
6) SIADH
Agent of choice to reduce BP after ICH
Nitroprusside
Stroke is associated with use of which illicit drug?
Cocaine
Given to reduce ICH after stroke
Mannitol and diuretics

*Do not use prophylactically
**DO NOT use steroids**
Pupillary findings in ICH
Pons: Pinpoint pupils
Thalamus: Poorly reactive pupils
Putamen: Dilated pupils
Common sites of SAH
1) Junction of anterior communicating artery with anterior cerebral artery
2) Junction of posterior communicating artery with internal carotid artery
3) Bifurcation of MCA
Causes of SAH
1) Ruptured Berry Aneurysm (MCC)
2) Trauma
3) AV malformation
Clinical features of SAH
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
Diagnosis of SAH
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
Complications of SAH
1) Rebleeding
2) Vasospasm
3) Hydrocephalus
4) Seizures
5) SIADH
Treatment of SAH
1) Surgical - clipping of aneurysm
2) Medical - to reduce risk of rebleeding and vasospasm (Ca2+ channel blocker)
Contraindication to lumbar puncture
Increased intracranial pressure

*Evidenced by papilledema
Characteristics of Parkinson's Disease
1) Loss of dopamine-containing neurons in pars compacta of substantia nigra (& locus ceruleus)
2) Essentially a clinical diagnosis
Clinical features of Parkinson's Disease
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
Shy-Drager Syndrome
Parkinsonian symptoms plus autonomic insufficiency
Medications associated with Parkinsonism
1) Neuroleptics
2) Metoclopramide
3) Reserpine
Treatment of Parkinson's Disease
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)
Side effects of Carbidopa-Levodopa
1) Dyskinesias (involuntary, choreic movements) --> reason for delayed tx
2) Levodopa has on-off fluctuations
Difference between Progressive Supranuclear Palsy (PSP) and Parkinson's
PSP does not cause tremor, but does cause ophthalmoplegia
Huntington's Chorea
Autosomal dominant mutation on chromosome 4
Expanded CAG repeats cause loss of GABA-producing neurons in STRIATUM
Clinical features of Huntington's Chorea
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
Diagnosis of Huntington's Chorea
1) MRI - atrophy of caudate nuclei
2) DNA testing
Treatment of Huntington's Chorea
1) Dopamine blockers help psychosis and chorea
2) Anxiolytics
3) Antidepressants

*There is no cure
3 Types of Tremor
1) Physiologic
2) Essential
3) Neurologic disease
Causes of Physiologic Tremor
1) Fear, anxiety, fatigue
2) Metabolic - HYPOglycemia, HYPERthyroidism, Pheochromocytoma
3) Toxic - EtOH withdrawl, valproic acid, lithium, caffeine, theophylline)
Treatment of Physiologic Tremor
Treat underlying cause
Essential Tremor
Autosomal dominant (33%)
Induced by intentional activity; Decreased with EtOH use
Treated with Propranolol
Characteristics of Ataxia
1) Gait instability
2) Loss of balance
3) Impaired limb coordination
Causes of Ataxia
1) Acquired - EtOH, vitamin B12 or thamine deficiency, cerebellar infarct, neoplasm, demyelinating disease, tabes dorsalis
2) Inherited - Friedreich's ataxia, Ataxia Telangiectasia
Friedreich's Ataxia
Autosomal recessive - onset in young adulthood
Ataxia, nystagmus, impaired vibration and proprioception
Ataxia Telangectasia
Autosomal recessive - childhood onset
Ataxia, nystagmus, impaired vibration and proprioception, telangectasias
*Increased incidence of cancer
Treatment of Ataxia
Treat underlying cause if possible
Psychiatric diagnosis associated with Tourette's Syndrome
Obsessive-Complusive Disorder
Clinical features of Tourette's
1) Motor tics
2) Vocal tics
Treatment of Tourette's Syndrome
1) Pimozide
2) Clonidine
3) Haloperidol
Dementia
Progressive deterioration of intellectual function with preservation of consciousness

*Most important risk factor is age
Differential diagnosis of Dementia
1) Primary neurologic disorder
2) Infection
3) Metabolic disorder
4) Drugs and toxins
5) Pseudodementia (depression)
Neurologic causes of dementia
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
Multi-infarct Dementia
Stepwise intellectual decline due to series of cerebral infarctions
Binswanger's Disease
Insidious onset of intellectual decline due to diffuse subcortical white matter degeneration

*Associated with long-standing HTN and atherosclerosis
Infectious causes of dementia
1) HIV (AIDS-related dementia)
2) Neurosyphilis
3) Cryptococcal infection
4) Creutzfeldt-Jakob disease
5) Progressive multifocal leukoencephalopathy
Metabolic causes of dementia
1) Thyroid disease (HYPO or HYPER)
2) Vitamin B12 deficiency
3) Thiamine deficiency (alcoholics)
4) Niacin deficiency
Laboratory studies to investigate cause of dementia
1) CBC with differential
2) CMP
3) TSH, T4
4) Vitamin B12, folate
5) VDRL
6) HIV
7) CT or MRI
Medical therapy for dementia
1) Vitamin E
2) Tacrine
3) Donepezil

*Evidence supporting these tx is inconclusive
Risk Factors for Alzheimer's Disease
1) Family hx
2) Down's Syndrome
Pathologic findings in Alzheimer's
1) Senile plaques - focal collections of dilated, tortuous neuritic processes surrounding central amyloid beta-protein
2) Neurofibrillary tangles - bundles of neurofilaments in nuclear cytoplasm
Early stage of Alzheimer's
Mild forgetfulness, impaired ability to learn new material, poor concentration, personality changes
Intermediate stage of Alzheimer's
Progressive memory impairment, visuospatial disturbances, verbal repetition
Late stage of Alzheimer's
Assistance needed for ADL, difficulty remembering names of family members, paranoid delusions and hallucinations
Imaging in Alzheimer's
Diffuse cortical atrophy with ventricle enlargement

*Clinical diagnosis
Treatment of Alzheimer's
1) AChE inhibitors - 1st line agent
2) Tacrine (QID)

*Vitamin E had benefit in one study
Delirium
Acute period of cognitive dysfunction due to medical disturbance or condition
Elderly pts especially prone
Causes of delirium
1) Postoperative state
2) Dehydration, drug intoxication
3) Infection, inflammation, fever
4) Medications, malnutrition, metals
5) Withdrawal states (EtOH, benzos)
6) Trauma, burns
Diagnosis of delirium
1) Mental status exam
2) Labs
3) LP - performed in any febrile, delirious pt
Treatment of delirium
1) Treat underlying cause
2) Haloperidol for agitation
Necessary for arousal and cognition
Arousal: Intact brainstem
Cognition: Intact cerebral cortex
Coma
Depressed level of consciousness such that pt is completely unresponsive to stimuli
Causes of coma
1) Structural brain lesions (usually bilateral)
2) Global brain dysfunction (metabolic or systemic disorders)
3) Psychiatric causes (conversion disorder)
Differential diagnosis of coma
S- Structural brain pathology
M- Meningitis, mental illness
A- Alcohol, acidosis
S- Seizures
H- Hypercapnia, hyperglycemia, hyponatremia, hypoxia
E- Endocrine, encephalitis, electrolytes
D- Drugs
Pupillary status associated with Uncal herniation
Anisocoria - asymmetric pupils
Pupillary status in severe anoxia
Bilateral, fixed, dilated pupils
Pupillary status with CN III compression
Unilateral, fixed, dilated pupil
Pupillary status with narcotic use or ICH
Pinpoint pupils
Oculocephalic test with intact brainstem
When head is turned to one side, eyes should move conjugately to the opposite side
Labs to do in pt in coma
CBC, electrolytes, Ca2+, BUN, ABGs, glucose, creatinine, EKG, toxicology
"Locked In" Syndrome
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*
Sites of Brain Herniation
1) Uncal (transtentorial) herniation
2) Tonsillar herniation
3) Central herniation
Uncal Herniation
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
Tonsillar Herniation
Medial portions of cerebellar hemispheres compress MEDULLA through foramen magnum
Compression of cardiopulmonary center can cause rapid death
Central Herniation
Supratentorial lesions
Cheyne-Stokes respirations, hyperventilation, extremity posturing, increased muscle tone, bilateral Babinski sign
Treatment of Brain Herniation
1) Intubation
2) Neurosurgery consult
3) Lower ICP
Multiple Sclerosis
Demyelination of CNS white matter and spinal cord

*Classically at angles of lateral ventricles
Tracts commonly affected by Multiple Sclerosis (MS)
1) Pyramidal and cerebellar pathways
2) Medial longitudinal fasciculus
3) Optic nerve
4) Posterior columns
Clinical features of MS
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
Optic Neuritis
Monocular vision loss
Pain on eye movement
Central scotoma (black spot)
Decreased pupillary reaction to light
Internuclear Ophthalmoplegia
Lesion in medial longitudinal Fasiculus
Ipsilateral medial rectus palsy on attempted lateral gaze and horizontal nystagmus

*Affected eye cannot adduct
Diagnostic test of choice for MS
MRI

*On LP, OLIGOCLONAL BANDS of IgG present in 90% of MS patients
Treatment of acute attacks of MS
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
Gullian-Barre Syndrome
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
Clinical features of Gullian-Barre Syndrome
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
Diagnosis of Gullian-Barre Syndrome
1) CSF - elevated protein, normal cell count
2) Electrodiagnostic studies - decreased motor nerve conduction velocity
Treatment of Gullian-Barre Syndrome
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**
MC intracranial neoplasm in adults
Brain Metastasis
MC primary CNS tumors in adults
1) Gliomas
2) Meningiomas
Clinical features of CNS Neoplasms
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)
Diagnosis of CNS Neoplasms
1) MRI with and without Gadolinium
2) Brain biopsy
Two important indications for MRI to rule out intracranial mass
1) New-onset seizure in adult
2) New and persistent or progressive headache
CNS tumors with good prognosis after resection
1) Meningioma
2) Schwannoma
3) Pituitary adenoma
CNS tumors unable to be resected
Gliomas (astrocytomas, oligodendrogliomas)

*Radiation may prolong survival
Astrocytomas
MC primary CNS neoplasm
Arise in cerebral hemispheres
Tend to cross corpus callosum into opposite hemisphere
Poor prognosis

*Glioblastoma Multiforme has worst prognosis*
Oligodendrogliomas
Peak occurrence between 40 - 50 years old
Malignant, but more indolent than fibrillary astrocytomas
*Survival: 10 - 15 years
Primary CNS Lymphoma
Related to immunosuppression
AIDS patients and transplant recipients highly susceptible
*5-year survival less than 5%
MC primary neoplasms that metastasize to the brain
1) Lung
2) Breast
3) Skin
4) Kidney
5) GI tract
Meningiomas
Extracerebral, well-defined round masses attached to the dura and compressing underlying brain

*Potential for surgical cure, but high recurrence
Schwannomas
Benign tumors (no malignant potential)
Bilateral --> pathognomonic for Neurofibromatosis Type II
Arise in cerebellopontine angle --> involves CN8 --> Hearing loss
Surgical resection achieves cure
Differential Diagnosis of Ring-Enhancing Brain Lesion
1) Metastatic CA
2) Brain Abscess
3) Glioblastoma Multiforme
4) Lymphoma
5) Toxoplasmosis
Meningeal Carcinomatosis
CA metastasis to meninges --> Focal deficits
CSF reveals malignant cells, elevated protein and lymphocytes and decreased glucose

*Treat with intrathecal chemotherapy
Secondary insults of Head Trauma
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
Most common cause of death after severe head injury
Increased intracranial pressure

*Normal ICP is 5-10mm H2O
*ICP > 20mm is worrisome
**Bilateral fixed and dilated pupils suggest diffusely increased ICP**
Signs of basilar skull fracture
1) Raccoon eyes
2) Battle sign
3) Otorhhea or CSF rhinorrhea
4) Hemotympanum
Cerebral Perfusion Pressure (equation)
Mean arterial pressure minus intracranial pressure

*Normal CPP is >50mm Hg
Key features of Head Trauma
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
Cushing's Triad
Physiologic response to increased ICP
1) Hypertension
2) Bradycardia
3) Respiratory irregularity

*If present, ICP is life-threatening
General techniques to lower ICP
1) Reverse Trendelenburg position
2) Intubation with hyperventilation
3) Mannitol
4) Lowering body temperature slightly
5) Draining CSF if ventricular catheter in place
Epidural Hematoma
Blood clot between skull and dura
Typically due to laceration of middle meningeal artery with temporal bone fracture
Clinical features of epidural hematoma
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
Subdural Hematoma
Blood clot between dura and the brain
Results from venous bleeding after blunt head trauma
*CT scan shows concave mass (crescent-shaped)
Risk factors for subdural hematoma
1) Brain atrophy (alcoholics and elderly patients)
2) Anticoagulated patients
Clinical features of acute subdural hematoma
Mass effect --> decline in mental status and change in level of consciousness
Poor prognosis
*Prompt surgical evacuation indicated
Clinical features of chronic subdural hematoma
Symptoms occur at least 1 week after injury
No loss of consciousness
May resolve if small
Typical findings with subdural hematomas
1) Decreased level of consciousness
2) Headache
3) Cortical dysfunction
Concussion
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
Myasthenia Gravis
Autoimmune disorder --> antibodies against nicotinic ACh receptors at neuromuscular junction
Reduced postsynaptic response and significant muscle fatigue
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)
Diagnosis of Myasthenia Gravis
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
Treatment of Myasthenia Gravis
1) AChE inhibitors - Pyridostigmine
2) THYMECTOMY
3) Immunosuppressive drugs (corticosteroids first)
4) Plasmapheresis removes antibodies
5) IVIG
6) Intubation if necessary
Medications that exacerbate Myasthenia Gravis symptoms
1) Aminoglycosides and tetracyclines
2) Beta-blockers
3) Anti-arrhythmics (Quinidine, Procainamide, Lidocaine)
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*
Duchenne's Muscular Dystrophy
X-lined recessive mutation in Dystophin gene
*No inflammation*
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
Diagnosis of Duchenne's Muscular Dystrophy
1) Serum creatinine phosphokinase levels
2) DNA testing
Treatment of Duchenne's Muscular Dystrophy
No treatment available
Predisone may slow progression
Surgery may correct scoliosis
Becker's Muscular Dystrophy
X-linked recessive mutation in Dystophin gene, but less severe than Duchenne's --> some dystrophin present
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
CNS tumors associated with NF1
1) Gliomas
2) Meningiomas
Complications of NF1
1) Scoliosis
2) Pheochromocytomas
3) Optic nerve gliomas
4) Renal artery stenosis
5) Erosive bone defects (spinal deformity, congenital tibial dysplasia)
Neurofibromatosis Type II
Autosomal dominant disorder
Bilateral acoustic neuromas (schwannomas), multiple meningiomas, neurofibromas, cataracts
Other features of Neurofibromatosis
1) Seizures
2) Mental retardation, learning disabilities
3) Short height
4) Macrocephaly
Tuberous Sclerosis
Autosomal dominant
Skin lesions (facial angiofibromas, adenoma sebaceum)
Cognitive impairment, epilepsy, retinal hamartomas, renal angiomyolipomas, cardiac rhabdomyomas
Sturge-Weber Syndrome
Acquired disorder
Capillary angiomatoses of pia mater
*Port-wine stain*
*Epilepsy and mental retardation*
Treatment of epilepsy is mainstay of treatment
Von Hippel-Lindau Disease
Autosomal Dominant
CAVERNOUS HEMANGIOMAS of brain or brainstem, renal angiomas, cysts in multiple organs
*Associated with Renal Cell Carcinoma*
Syringomyelia
Central cavitation of CERVICAL spinal cord --> abnormal fluid collection w/in cord parenchyma
*Diagnosed by MRI
*Treated by surgical syringosubarachnoid shunt
Causes of syringomyelia
1) Cranial base malformation (Arnold-Chiari malformation)
2) Intramedullary tumors
3) Traumatic necrosis of cord
Clinical features of Syringomyelia
Bilateral loss of PAIN & TEMPERATURE over shoulders (capelike distribution) --> Lateral Spinothalamic Tract

*Muscle atrophy of hands may occur
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)
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
Horner's Syndrome
1) Miosis
2) Anhydrosis
3) Ptosis

*Interruption of cervical sympathetic nerves
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)
Poliomyelitis
Poliovirus damage to anterior horn cells and motor neurons of spinal cord and brainstem --> LMN signs
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
3 major causes of Dizziness
1) Presyncope (lightheadedness)
2) Vertigo
3) Multisensory stimuli (sensory overload)
Vertigo
Disturbance of vestibular system --> sensation of spinning or hallucination of movement
Peripheral (benign) or central
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
Meniere's Disease
Triad of
1) Vertigo
2) Tinnitis
3) Hearing loss

*Attacks wax and wane; hearing loss eventually becomes permanent
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)
Causes of Central Vertigo
1) Multiple Sclerosis
2) Vertebrobasilar insufficiency
3) Migraine-associated vertigo (w/ or w/o headache)
Syncope
Transient loss of consciousness/postural tone 2/2 acute decrease in cerebral blood flow
Rapid recovery of consciousness w/o resuscitation
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)
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
Vasovagal Syncope
MCC of syncope
Precipitated by emotion, pain, fear, claustrophobic situations
Tilt-table study reproduces symptoms
Medical treatment of vasovagal syncope
1) Beta-blockers
2) Disopyramide
Treatment of Orthostatic Syncope
1) Increased salt intake and fluids
2) Fludrocortisone
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
Physical exam in evaluation of syncope
1) Orthostatic BPs and pulse
2) Mental status (post-ictal state)
3) Murmurs
4) Carotid pulses
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
Seizure
Sudden abnormal discharge of electrical activity in the brain
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
Metabolic causes of seizure
1) HYPOnatremia
2) HYPOcalcemia
3) HYPO or HYPERglycemia
4) HYPERthermia
5) Uremia
6) Thyroid storm
7) Water intoxication
Simple Partial Seizure
*Consciousness remains intact*
Localized, but may evolve to be complex
*May involve transient, unilateral clonic-tonic movement
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
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*
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
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
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