Neurology Flashcards
cerebrum
CORTEX:
fx in higher brain processes like thought/action, controls all voluntary activity (w/ help of the cerebellum)
-Frontal: reasoning, problem solve, parts of speech, mvmt, emo
-Parietal: perception/recognition of stimuli, orientation, mvmt
-Temporal: memory, perception/recognition of auditory stimuli and speech
-Occipital: visual processing
BASAL GANGLIA:
voluntary motor mvmt, coordination, cognition, emotion
LIMBIC SYSTEM:
thalamus, hypothalamus, amygdala and hippocampus
-Amygdala: located in temporal lobe, involved in memory, emo and fear
-Hippocampus: learning, memory; converts short-term into long-term memory
diencephalon
THALAMUS:
- located deep in the forebrain
- processes nearly all sensor and motor info
- relays info to/from cortex
HYPOTHALAMUS:
- located below and ventral to thalamus
- controls homeostasis
brainstem
MIDBRAIN:
controls eye mvmt, relays visual and auditory info
PONS:
REGULATES BREATHING, SERVES AS A RELAY STATION BTW CEREBRAL HEMISPHERE AND MEDULLA
-involved in motor control and sensory input
MEDULLA OBLONGATA:
extension of spinal cord
-regulates vital body fx such as heart rate, breathing, autonomic centers, swallowing and coughing
cerebellum
posterior to medulla
maintains posture and balance, coordinates voluntary mvmt and controls certain head and eye mvmt
basal ganglia disorders
EXTRAPYRAMIDAL SYMPTOMS:
- Dyskinesia
- Dystonia - sustained contraction, twisting abn position
- Myoclonus - invol jerk/twitch
- Tics - suppressible
- Chorea - rapid invol jerky, uncontrolled, purposeless
- Muscle spasms - tonic (sustained rigid) or clonic (repeat, rapid)
- Tremors
PARKINSONISM
- Parkinson Disease
- Dopamine antagonists (haloperidol, olanzapine, risperidone, promethazine, metoclopramide)
- Lewy body disease - loss of dopaminergic neurons, anticholinergic neurons
- Other: head trauma, HIV, carbon mo, mercury poisoning, cns dysfunction
Huntington disease
huntington gene –> neurotoxicity as well as cerebral, putamen and caudate nucleus atrophy
- sx:
- Behavioral: personality, cognitive, intellectual and psych including irritability
- Chorea: rapid, invol or arrhythmic mvmt of face, neck, trunk and limbs initially; worse w/ vol mvmts and stress
- Dementia: most devo dementia before 50y (primarily exec fx)
- gait abnormalities/ataxia, incontinence, facial grimacing
- brisk DTR
-dx:
CT: CEREBRAL AND CAUDATE NUCLEUS ATROPHY
PET: dec glucose metabolism in caudate nucleus and putamen
- tx:
- usually fatal w/in 15-20y after presentation
- CHOREA MANAGEMENT: antidopinergics: typical/atypical antipsychotics, tetrabenazine, benzos
essential familial tremor
-AUTO DOM, onset usually in 60s
- sx:
- INTENTIONAL TREMOR - POSTURAL, BILATERAL ACTION TREMOR OF HANDS, FOREARMS, HEAD, NECK OR VOICE
- mc in upper extremities and head
- WORSE W/ EMO STRESS AND INTENTIONAL MVMT
- SHORTLY RELIEVED W/ ETOH INGESTION
- normal neuro exam otherwise
- tx
- PROPANOLOL MAY HELP SEVERE OR SITUATIONAL
- Primidone (barbiturate) if no relief or instead of propanolol
- Alprazolam (benzo) 3rd line
parkinson disease
IDIOPATHIC DOPAMINE DEPLETION –> failure to inhibit acethylcholine in basal ganglia (Ach is excitatory nt and dopamine is inhibitory)
- onset 45-65 mc
- LEWY BODIES (cytoplasmic inclusions), LOSS OF PIGMENT CELLS SEEN IN SUBSTANTIA NIGRA
- sx:
- RESTING TREMOR MC SIGN (PILL ROLLING) - worse w/ rest and emo stress; less w/ voluntary activity/intentional movement, usually starts w/ one limb for years until generalized
- BRADYKINESIA - slow vol mvmt, dec automatic mvmt
- RIGIDITY - inc resist to passive mvmt (COGWHEEL); festination = increasing speed while walking, norm DTR
- FACE INVOLVEMENT - FIXED FACIAL EXPRESSIONS, widened palpebral fissure; MYERSON’S SIGN: tapping bridge of nose repetitively causes a sustained blink
- POSTURAL INSTABILITY - usually late finding, “pull test”
- dementia in 50% (late finding)
- tx:
- drug tx not used initially if sx mild
- LEVODOPA/CARBIDOPA - MOST EFFECTIVE - levo converted into dopamine (carbidopa reduces amt of levo needed, reducing SE)
- DOPA AGONISTS: BROMOCRIPTINE, PRAMIPEXOLE, ROPINEROLE - stimulate dopamine receptors; sometimes used in young pt to delay use of levodopa
- ANTICHOLINERGICS: TRIHEXYPHENIDYL, BENZTROPINE - blocks excitatory cholinergic effects
- Amantadine - inc pre-synaptic dopa release
- MAO-B Inhibitors - inc dopa
tourette syndrome
-onset usually childhood (2-5y), mc boys
+/- assoc w/ obsessions-compulsions
- sx:
- MOTOR TICS of face, head, neck
- VERBAL OR PHONETIC TICS: grunts, throat clearing, obscene words (coprolalia), repeating others (echolalia)
- self-mutliating tics: hair pull, nail bite, bite lips
- tx:
- HABIT REVERSAL THERAPY - 50% REVERSE BY 18
- Dapamine-blocking agents: HALOPERIDOL, RISPERIDONE
- Alpha-adrenergics: CLONIDINE, GUANFACINE, clonazepam as adjunct
amyotrophic lateral sclerosis (ALS)
-necrosis of BOTH upper and lower motor neurons –> PROGRESSIVE MOTOR DEGENERATION
- sx:
- muscle weakness, LOSS OF ABILITY TO INITIATE AND CONTROL MOTOR MVMT
- MIXED UPPER AND LOWER MOTOR NEURON SIGNS
- Upper: spasticity, stiffness, hyperreflexia
- Lower: progressive bilateral fasciculations, muscle atrophy, hyporeflexia, muscle weakness
- bulbar sx: dysphagia, dysarthria, speech problems, eventual respiratory dysfunction
- SENSATION, URINARY SPHINCTER AND VOLUNTARY EYE MOVEMENTS ARE SPARED
- tx:
- RILUZOLE reduces progression for up to 6 mo
- usually fatal w/in 3-5 years of onset
cerebral palsy
-CNS disorder assoc w/ muscle tone and postural abnormalities due to brain injury during perinatal or prenatal period
- sx:
- SPASTICITY HALLMARK - varying degrees of motor deficits, often assoc w/ intellectual/learning disabilities and devo abnormalities
- HYPERREFLEXIA, limb-length discrepancies, congenital defects
- tx:
- multidisciplinary approach
- spasticity –> Baclofen, Diazepam, antiepileptics for seizures
restless legs syndrome (Willis-Eckbom disease)
-sleep-related mvmt disorder; usually primary but may occur secondary to cns Fe deficiency, pregnancy, peripheral neuropathy
- dx:
- uncomfortable or unpleasant sensation (itching, burning, paresthesias, etc) in the leg that creates an urge to move the legs
- worse at night, tends to occur w/ prolonged periods of rest or inactivity
- improves w/ movement
- tx:
- DOPAMINE AGONIST TX OF CHOICE: PRAMIPEXOLE, ROPINIROLE
- Alpha-2-Delta Calcium channel ligands: GABA, PREGAB
- Benzos
- Opioids in disease resistant to above
- FE SUPPLEMENT REC IN PT W/ SERUM FERRITIN LOWER THAN 75mcg/L bc of assoc w/ Fe deficiency in cns
guillain barre syndrome
- acute/subacute acquired inflammatory DEMYELINATING POLYRADICULOPATHY of PERIPHERAL NERVES
- INC INCIDENCE W/ CAMPYLOBACKER JEJUNI MC or other antecedents RESPIRATORY OR GI INFX (CMV, EBV, HIV, mycoplasma, immunizations, postsurgical)
-Patho: immune-med demyelination and axonal degeneration slows nerve impulses –> symmetric weakness and paresthesias; post infx immune response cross-reacts w/ peripheral nerve components
- sx:
- ASCENDING WEAKNESS AND PARESTHESIAS (usually symmetric)
- DEC DTR (lower motor neuron), may involve muscles of respiration or bulbar muscles (swallowing), CNVII palsy
- AUTONOMIC DYSFUNCTION: tachy, hypoTN/hyperTN, BREATHING DIFFICULTIES
- dx:
- CSF: HIGH PROTEIN W/ NORMAL WBC (high protein after 1-3 wks of sx)
- Electrophysicoligc studies: dec motor nerve conduction
- tx:
- PLASMAPHERESIS best if done early - removes harmful auto-ab, equally effective as IVIG
- IVIG: suppress harmful inflam/auto-ab and induces remyelination; most recover w/in months
- mech vent if respiratory failure
- PREDNISONE CONTRAINDICATED
- PROGNOSIS: 60% FULL RECOVERY IN 1 YR, 10-20% left w/ permanent disability
myasthenia gravis
AUTOIMMUNE peripheral nerve disorder; HLA-DR3
MC YOUNG WOMEN
75% have THYMIC ABNORMALITY (HYPERPLASIA OR THYMOMA) or other immune disorders
-Patho: inefficient skeletal muscle neuromusclar transmission d/t AUTOAIMMUNE AB AGAINST ACETYLCHOLINE (NICOTINIC) POSTSYNAPTIC RECPTOR at neuromuscular jx (dec ACh receptors)
-sx:
OCULAR: usually 1st presenting
-extraocular involvement –> DIPLOPIA, PTOSIS/eyelid weakness (more prominent w/ upward gaze) weakness worse w/ repeated use, pupils spared
GENERALIZED: WORSE MUSCLE WEAKNESS W/ REPEATED USE THROUGHOUT DAY (relieved w/ rest)
-normal sensation and DTR
-BULBAR WEAKNESS (oropharyngeal) w/ prolonged chewing, dysphagia
-RESPIRATORY MUSCLE WEAKNESS may lead to RESPIRATORY FAILURE = MYASTHENIC CRISIS**
-dx:
+ ACETYLCHOLINE RECEPTOR ANTIBODIES
+ MuSK (muscle-specific tyrosine kinase) AB
-EDROPHONIUM (TENSILON) TEST: rapid response to short-acting IV Edrophonium
-CT scan or MRI of chest may show THYMOMA or THYMUS GLAND ABNORMAL
-ICE PACK TEST –> eyelid 10 min –> improve ptosis
- tx:
- ACETYLCHOLINESTERASE INHIBITORS: PYRIDOSTIGMINE OR NEOSTIGMINE 1ST LINE –> inc ACh (dec breakdown), SE: CHOLINERGIC CRISIS (weak, n/v, sweat, salivation, diarrhea, miosis, brady, resp failure)
- IMMUNOSUPPRESSION: PLASMAPHERESIS OR IVIG for myasthenic crisis
- Chronic: CORTICO
- THYMECTOMY if thymoma
- AVOID FLUOROQUINOLONES AND AMINOGLYCOSIDES
CRISIS:
- IF FLACCID PARALYSIS IMPROVES W/ TENSILON –> MYASTHENIC CRISIS
- IF FLACCID PARALYSIS WORSENS W/ TENSILON –> CHOLINERGIC CRISIS
- ddx:
- MYASTHENIC SYNDROME (LAMBERT-EATON) MC ASSOC W/ SMALL CELL LUNG CA –> WEAKNESS IMPROVES W/ USE
multiple sclerosis
AUTOIMMUNE, INFLAMMATORY DEMYELINATING DISEASE of IDIOPATHIC ORIGIN
-MC WOMEN AND YOUNG ADULTS 20-40Y
- RELAPSE-REMITTING MC episodic exacerbations
- Progressive: decline w/out acute exacerbations
- Secondary progressive: relapse-remitting that becomes progressive
- sx:
- Sensory Deficits: pain, fatigue, numbness, paresthesias in limbs, TRIGEMINAL NEURALGIA, UHTHOFF’S PHENOMENON (worsening of sx w/ heat), LHERMITTE’S SIGN
- OPTIC NEURITIS (RETROBULBAR) unilateral eye pain worse w/ movement, diplopia, central scotomas, VL
- MARCUS-GUNN PUPIL: swinging flashlight from unaffected to affected –> pupils appear to dilate
- MOTOR: UPPER –> SPASTICITY AND + BABINSKI
- spinal cord sx: bladder, bowel or sexual dysfunction
- CHARCOT’S NEUROLOGIC TRIAD: nystagmus, staccato speech, intentional tremor
-dx:
-mainly clinical - at least 2 discrete episodes of exacer
-MRI W/ GADOLINIUM - TEST OF CHOICE TO CONFIRM
WHITE MATTER PLAQUES (hyperdensities) hallmark
-LUMBAR PUNCTURE: INC IgG (OLIGOCLONAL)
- tx:
- ACUTE: IV CORTICO 1ST LINE, plasmapheresis
- RELAPSE/REMIT/PROGRESSIVE: B-INTERFERON or GLATIRAMER ACETATE decrease #/severity of relapse
- amantadine is helpful for fatigue, baclofen and diazepam for spasticity
bell palsy
IDIOPATHIC, UNILATERAL CN 7/FACIAL NERVE PALSY d/t inflammation or compression
- lower motor neuron lesion, MC RIGHT SIDE
- STRONG ASSOC W/ HSV REACTIVATION
-RF: Dm, pregnancy (esp 3rd tri), post URI, dental nerve block
- sx:
- sudden onset of IPSILATERAL HYPERACUSIS (EAR PAIN) 24-48h –> UNILATERAL FACIAL PARALYSIS, UNABLE TO LIFT AFFECTED EYEBROW
- TASTE DISTURBANCE ANTERIOR 2/3
- ONLY AFFECTS FACE
-dx: of exclusion
-tx:
-most resolve w/in 1 month w/out tx
-PREDNISONE (ESP W/IN 72H)
-ARTIFICIAL TEARS
+/- Acyclovir
- DDx:
- upper motor lesions (cva)
- IF UPPER FACE OK (wrinkle forehead) – NOT BELLS PALSY
headaches - general
PRIMARY (90%): MIGRAINE, TENSION, CLUSTER OR REBOUND - IDIOPATHIC
SECONDARY (4%): meningitis, subarachnoid hemorrhage, intracranial htn, acute glaucoma (suspect if abrupt or progression of severity)
tension headache
mc overall type
-ave age onset 30y, thought to be d/t mental stress
- sx:
- BILATERAL, TIGHT, BAND-LIKE, constant daily
- worse w/ stress, fatigue, noise or glare
- not usually pulsatile
- NO N/V, FOCAL NEURO SX (no photophobia)
- tx:
- treat like migraines; 1st line: NSAIDs, asa, tylenol, anti-migraine meds
- TCAs (amitriptyline) in severe/recurrent, prophylaxis, BB
migraine headache
- mc women, mc cause of morning ha, family hx 80%
- 2 TYPES: W/OUT AURA (COMMON) AND W/ AURA
- thought to be caused by vasodilation of blood vessels innervated by the trigeminal nerve
- sx:
- LATERALIZED, PULSATILE/THROBBING HA, ASSOC W/ N/V, PHOTOPHOBIA usually 4-72h duration, +/-bilat
- WORSE W/ PHYSICAL ACTIVITY, stress, lack/excessive sleep, etoh, foods (choc, red wine), OCPs, menstruation
- AURAS: VISUAL CHANGE MC - light flashes (photopsia), zig-zag light (teichopsia), scotomas, aphasia, weak, numb
-tx:
Symptomatic:
-TRIPTANS OR ERGOTAMINES (serotonin 5HT-1 agonists –> vasoconstrict) c/i CAD, PVD, uncontrolled HTN, hepatic, renal dz, pregnancy
-DOPAMINE BLOCKERS (metoclopramide, promethazine, prochlorperazine) as ANTIEMETICS, GIVE W/ BENADRYL TO PREVENT EPS
-iv fluids, dark room
-mild: NSAIDs/tylenol 1st line
Prophylactic:
-ANTI-HTN (BB, CCB), tca, anticonvulsants (valproate, topiramate)
trigeminal neuralgia
compression of trigeminal nerve root (by superior cerebellar artery or vein) 90%, idiopathic 10%
-mc middle-aged women
- sx:
- BRIEF, EPISODIC, STAB/LANCINATING PAIN in 2nd/3rd division of TRIGEMINAL NERVE (cn 5) lasts sec-min
- WORSE W/ TOUCH, EATING, DRAFTS OF WIND, MOVEMENTS (OFTEN UNILATERAL)
- starts near mouth and shoots to eye, ear and nostril on ipsilateral side
- tx:
- CARBAMAZEPINE (TEGRETOL) 1ST LINE, oxcarbazepine
- GABAPENTIN
- sx decompression in severe cases
*suspect MS in younger pt w/ TGN
cluster headache
-young/middle-aged males mc
- sx:
- SEVERE, UNILATERAL PERIORBITAL/TEMPORAL PAIN (SHARP, LANCINATING)
- LASTS <2 HR w/ spontaneous remission
- several times/day over 6-8 wks
- WORSE AT NIGHT, ETOH, STRESS OR FOODS
- IPSILATERAL HORNER’S SYNDROME (ptosis, miosis, anhydrosis), HASAL CONGESTION/RHINORRHEA, CONJUNCTIVITIS AND LACRIMATION
- tx:
- 100% O2 FIRST LINE
- ANTI MIGRAINE MEDS - SQ SUMATRIPTAN or ergotamines
- Prophylaxis: VERAPAMIL 1ST LINE, cortico, ergotamines, valproic acid, lithium
idiopathic intracranial htn (pseudotumor cerebri)
IDIOPATHIC INC INTRACRANIAL (CSF) PRESSURE and no other cause of intracranial htn evident on ct/mri
-mc in obese women of childbearing age, cortico w/drawal, growth hormone, thyroid replacement, ocp
- sx:
- HEADACHE (worse w/ strain), retrobulbar pain, n/v, tinnitus, VISUAL CHANGE (can lead to blindness)
-dx:
-PAPILLEDEMA
+/- CN6 (abducens) palsy = lateral rectus muscle weakness –> limits of abduction
-CT SCAN: 1ST TO R/O MASS –> LP = INC CSF PRESSURE
- tx:
- ACETAZOLAMIDE (reduces csf pressure/production) +/- furosemide, +/- short course steroids
- optic nerve sheath fenestration of CSF shunting allows evacuation of csf
CSF Findings
MS = high IgG (oligoclonal bands)
GB = high protein, normal WBC
Bacterial = high protein w/ inc WBC (PMNs), dec glucose
Viral = normal glucose, increased WBCs (lymph)
Fungal / TB = decreased glucose, increased WBC (lymph)
Idiopathic Intracranial HTN = increased CSF pressure
Subarachnoid Hemorrhage = xanthochromia, blood in CSF
*IF GLUCOSE NORMAL, VIRAL MENINGITIS MOST LIKELY, IF PMNS PREDOMINANT, BACTERIAL MOST LIKELY
normal pressure hydrocephalus
- dilation of cerebral ventricles w/ normal opening pressures on lumbar puncture
- unknown, thought to be d/t impaired CSF absorption after injury (SAH, tumors, infx, inflam, trauma)
-sx:
TRIAD:
-GAIT DISTURBANCES - wide base, shuffling gait
-DEMENTIA - impaired exec fx, psychomotor depression
-URINARY INCONTINENCE - urgency early in dz
-other: weakness, lethargy, malaise, rigidity, hyperreflexia and spasticity
- dx:
- MRI/CT: ENLARGED VENTRICLES in absence or out or proportion to sulcal dilation (MRI pref)
- LP: CSF usuall normal; lumbar tap test = remove up to 50 cc leads to improvement 30-60 min after
- tx:
- VENTRICULOPERITONEAL SHUNT TX OF CHOICE
concussion
-mild traumatic brain injury –> alteration of mental status w/ or w/out loss of consciousness
- sx:
- CONFUSION, blank expression, blunted affect
- AMNESIA: pre-traumatic (retrograde) or post-traumatic (antegrade)
- headache, dizzy, visual disturbances: blurry/double
- delated responses and emo changes
- signs of inc intracranial pressure: persistent vomiting, worsening headache, inc disorientation, changing levels of consciousness
- dx:
- CT TEST OF CHOICE
- MRI if prolonged sx >7-14d or w/ worsening of sx not explained by concussion
- tx:
- COGNITIVE AND PHYSICAL REST
- pt may resume activity after resolution of sx and recovery of memory/cog fx
delirium
ACUTE, ABRUPT, TRANSIENT CONFUSED STATE d/t an IDENTIFIABLE CAUSE (MEDS, INFX)
- rapid onset assoc w/ fluctuating mental status changes and marked deficit in short-term memory
- recovery w/in 1 week most cases
dementia
PROGRESSIVE, CHRONIC INTELLECTUAL DETERIORATION
- MEMORY LOSS and loss of impulse control, motor and cognitive fx
- includes language dysfx, disorientation, inability to perform complex motor activity and inappropriate social interactions
- RF: age (esp >60) and vascular disease
- Includes: alzheimer’s, vascular, frontotemporal, diffuse lewy body, creutzfeldt-jakob
Alzheimer disease
MC TYPE OF DEMENTIA
- AMYLOID DEPOSITION (SENILE PLAQUES)
- NEUROFIBRILLARY TANGLES (TAU PROTEIN)
- CHOLINGERGIC DEFICIENCY –> memory, language, visuospatial changes, normal reflexes
- sx:
- short-term memory loss (1st sx) progresses to long term, disorientation, behavioral and personality changes
- dx:
- CT SCAN - CEREBRAL CORTEX ATROPHY
- tx:
- AcH-ESTERASE INHIBITORS: DONEPEZIL, TACRINE, RIVASTIGMINE, GLANTAMINE (reverse cholinergic deficiency and sx relief - doesn’t slow)
- NMDA ANTAGONIST: MEMANTINE (blocks nmda receptor, slow Ca influx and nerve damage) –> reduce glutamate excitotoxicity
vascular dementia
2nd MC TYPE
- BRAIN DZ D/T CHRONIC ISCHEMIA AND MULTIPLE INFARCTIONS (LACUNAR INFARCTS)
- HTN MOST IMPORTANT RISK FACTOR
- sx:
- Cortical: forgetfulness, confusion, amnesia, exec difficulties, speech abn
- Subcortical: motor deficits, gait abnormalities, urinary difficulties, personality changes
frontotemporal dementia (Pick’s disease)
-rare type
-LOCALIZED BRAIN DEGENERATION OF FRONTOTEMPORAL LOBES
-MARKED PERSONALITY CHANGES (PRESERVED VISUOSPATIAL)
-apathy, disinhibition, +palmomental and palmar grasp reflexes, no amnesia
+PICK BODIES
diffuse lewy body disease
- lewy bodies: abn neuronal protein deposits (diffuse in comparison to parkinson’s dz - local)
- VISUAL HALLUCINATIONS, DELUSIONS, episodic delirium, parkinsonism
- dementia later in dz course
upper motor neuron lesions
- UMN connects cortex to LMN (in spinal cord)
- nt glutamate transmits nerve impulses from upper motor to lower motor neurons
- etiologies:
- stroke
- MS
- cerebral palsy
- brain or spinal cord damage (tbi)
- SPASTIC PARALYSIS (HYPERTONIA)
- INCREASED DTR
- weakness
- no fasciculations
- UPWARD (POS/ABN) BABINSKI
- little/no muscle atrophy
lower motor neuron lesions
- LMN are located in spinal cord and links UMN to muscles
- LMN stim by glutamate release from UMN causing depolarization of LMN
- LMN terminates at effector (muscle); AcH RELEASE BY LMN STIMULATES MUSCLE CONTRACTION
- etiologies:
- guillain-barre
- botulism
- poliomyelitis
- cauda equina
- bell palsy
- FLACCID PARALYSIS (LOSS OF TONE / HYPOTONIA)
- DECREASED DTR
- weakness
- FASCICULATIONS
- DOWNWARD (NEG/NORM) BABINSKI
- MUSCLE ATROPHY
glasgow coma scale
eye-opening 1-4
verbal response 1-5
motor response 1-6
mild injury 13+
mod injury 9-12
severe injury = 8
astrocytoma
- derived from astrocytes (support endothelial cells ob BBB, provide nutrients for cells, maintain extra cellular ion balance)
- can appear in any part of brain
Types:
-PILOCYTIC ASTROCYTOMA (GRADE I) - juvenile, typically localized, MOST BENIGN, MC CHILDREN AND YOUNG ADULTS
- DIFFUSE ASTROCYTOMA (GRADE II) - tend to invade surrounding tissues but grow at slow pace
- ANAPLASTIC ASTROCYTOMA (GRADE III) - rare but aggressive
- GRADE IV ASTROCYTOMA = GLIOBLASTOMA MULIFORME - MC PRIMARY CNS TUMOR ADULTS
- sx:
- FOCAL DEFICITS MC - depends on location, mc in frontal and temporal areas
- general: ha, worse in morning, MAY WAKE PT UP AT NIGHT, cranial nerve deficits, ams, ataxia, vision change
- INCREASED INTRACRANIAL PRESSURE - MASS EFFECT
- dx:
- CT OR MRI W/ CONTRAST: grade I+II non-enhancing
- BX: pilocytic, diffuse, anaplastic, glioblastoma (may contain cystic material, calcium, bv)
- tx:
- Pilocytic: surgical excision +/-radiation
- Diffuse: sx if accessible +/- radiation
- Anaplastic: sx –> radiation +/-chemo after
- Glioblastoma: sx –> radiation + chemo
glioblastoma
MC AND MOST AGGRESSIVE PRIMARY TUMOR ADULTS
- GRADE IV ASTROCYTOMA
- PRIMARY MC (60%) SEEN IN ADULTS >50Y
- SECONDARY (40%) due to malignant progression from low-grade astrocytoma or anaplastic astrocytoma (grade III); may transform as early as 1 year or >10y
- RF: male, >50y, HHV-6, CMV, ionizing radiation
- sx:
- focal deficits mc, depends on location (mc frontal, temporal)
- ha, worse in morning, MAY WAKE PT UP AT NIGHT, cranial nerve deficits, ams, ataxia, vision change
- Frontal: dementia, personality change, gait, aphasia
- Temporal: partial complex and general seizures
- Parietal: contralateral sensory loss, hemianopia
- Occipital: contralateral homonymous hemianopia
- Thalamus: contralateral sensory loss
- Brainstem: papillary changes, nystagmus, hemiparesis
- INC INTRACRANIAL PRESSURE - MASS EFFECT: ha, n/v, papilledema, ataxia
- CUSHING’S REFLEX: IRREGULAR RESPIRATIONS, HTN, BRADYCARDIA
- dx:
- CT or MRI w/ contrast - mc seen in subcortical white matter of cerebral hemis –> nonhomogenous mass w/ hypodense center and VARIABLE RING OF ENHANCEMENT; MAY CROSS CORPUS CALLOSUM
- BX: small areas of NECROTIZING TISSUE surrounded by anaplastic cells and hyperplastic bv w/ areas of HEMORRHAGE
- tx:
- surgical excision, radiation and chemo w/ Temozolomide
- poor prognosis –> often <1 yr survival
meningiomas
USUALLY BENIGN, 2nd MC CNS PRIMARY NEOPLASM
- mc women (estrogen receptors on tumor cells)
- ASSOC W/ NEUROFIBROMATOSIS (ESP 2)
- MC ARISE FROM DURA OR SITES OF DURAL REFLECTION
- sx:
- most asymptomatic, found incidentally
- focal deficits: seizures, progressive spasticity, weakness or other motor/sensory sx
- dx:
- CT or MRI w/ contrast: INTENSELY ENHANCING, WELL-DEFINED LESION OFTEN ATTACHED TO DURS
- mc parasagittal region, convexities of hemis, sphenoid and olfactory groove, calcification
- BX: SPINDLE-CELLS concentrically arranged in WHORLED PATTERN; PSAMMOMA BODIES: concentric round calcifications
- tx:
- observe if asymptomatic/small
- surgical removal or radiation if not candidate
cns lymphoma
- Primary: seen w/out evidence of systemic dz; VARIANT OF EXTRANODAL NHL
- Secondary: mc, mets from another site (ex NHL in neck, chest, groin, abdomen) ESP DIFFUSE LARGE B CELL LYMPHOMA (90%), BURKITT’S LYMPHOMA (10%)
- RF: immunosuppression, EBV+ in 90%
- sx:
- focal deficits mc; depends on location
- ocular sx: visual change, steroid-refractory posterior uveitis
- dx:
- CT/MRI w/ contrast: hypointense RING-ENHANCING LESION in deep white matter on CT
- BX
- workup: CT of abd/pelvis, PET scan, BM bx, slit lamp
- tx:
- CHEMO: METHOTREXATE MOST EFFECTIVE
- RADIATION, CORTICO
- surgical resection usually ineffective
oligodendoglioma
oligodendrocyte - supportive (glial) tissue of brain
- sx:
- may be asymptomatic, incidental finding (slow growth)
- focal deficits: seizures, ha, personality change (depends on location)
- dx:
- CT/MRI w/ contrast
- BX: soft, gray-ish, pink CALCIFIED tumors, areas of hemorrhage and or cystic; CHICKEN-WIRE CAPILLARY PATTERN W/ FRIED EGG SHAPED tumor cells
-tx:
-surgical resection tx of choice
+/- radiation and/or chemo
ependyoma
- ependymal cells line ventricles and parts of spinal column
- MC IN CHILDREN, MC IN 4TH VENTRICLE, +/- medulla, spinal cord
- sx:
- Infants: inc head size, irritability, sleeplessness, vomiting
- Older children: n/v, headache
- dx:
- CT/MRI w/ contrast: hypointense T1, hyperintense T2, enhances w/ gadolinium
- BX: PERIVASCULAR PSEUDOROSETTES (tumor cells surrounding a blood vessel)
- tx:
- surgical resection –> radiation tx
hemangiomas
- abnormal buildup of bv in skin or internal organs
- 10% have Hippel-Lindau syndrome (+ tumors of liver, pancreas and kidney)
- HEMANGIOBLASTOMA: arises from blood vessel lining; benign, slow-growing well-definited tumors
- mc found in BRAINSTEM AND CEREBELLUM
- RETINAL HEMANGIOMAS ASSOC W/ VON HIPPEL-LINDAU SYDROME
- sx:
- Hemangioblastoma: ha, n/v, gait, poor coordination, may produce epo
- Hemaiopericytoma: depends on location
- dx:
- CT/MRI w/ contrast
- BX: well-defined borders, FOAM CELLS W/ HIGH VASCULARITY
- tx:
- surgical resection, radiation may be used in tumors attached to brainstem
atlas C1 burst fracture (Jefferson)
BILATERAL FRX OF ANTERIOR AND POSTERIOR ARCHES OF C1
+/- C1/C2 dislocation
MOI: vertical compression force through occipital condyles to the lateral masses of the atlas
- dx:
- lateral xray –> inc predental space btw C1 and odontoid (dens)
- open-mouth (odontoid) view: may show step-off
- tx:
- nonoperative: hard cervical orthosis vs halo immobilization 6-12 wks
- operative: posterior C1-C2 fusion vs occipitocervical fusion if unstable
hangman’s (C2/axis pedicle) fracture
TRAUMATIC BILAT FRX (SPONDYLOLYSIS) OF PEDICLES OR PARS INTERARTICULARIS OF THE AXIS VERTEBRA (C2) –> may lead to spondylolisthesis btw C2 and C3
-UNSTABLE FRX
- MOI: extreme hyperextension injuries of skull, atlas and axis (esp in already extended neck) and secondary flexion w/ subsequent subluxation
- sx: neck pain, neuro exam intact (cervical canal wide)
- dx:
- Cervical XRAY: subluxation (slipping of C2 forward compared to C3)
- CT - STUDY OF CHOICE (mri if artery injury suspected)
- tx:
- nonoperative: type I (<3mm displace) rigid collar 4-6wk, type II (3-5mm) closed reduction followed by halo immobilization 8-12wk
- operative: type II (>5mm w/ severe angulation)
odontoid fractures
-fracture of dens (odontoid process) of axis (c2)
MOI: head placed in forced flexion or extension in ant-pos orientation) - ex forward fall onto forehead
- Type II: MC - fracture at base of dontoid process (dens) where it attaches to C2; UNSTABLE
- dx: best seen on AP odontoid (open mouth) view
- tx:
- Os odontoideum (aplasia or hypoplasia of odontoid) –> observe
- Type II in young –> halo, sx if RF for nonunion
- Type II in elderly –> sx preferred; orthosis if not candidate
- Type III –> cervical orthosis
atlas fracture and transverse ligamental instability
MOI:
- hyperextension and compression injuries
- low risk of neuro complications; may be assoc w/ axis frx
atlanto-occipital dislocation
-extreme flexion injury involving atlas (C1) and axis (C2)
+/- assoc w/ odontoid frx
atlanto-axial joint instability
instability btw atlas (C1) and axis (C2)
MOI:
- Trauma: d/t extreme flexion-rotation injury
- Non-trauma: degnerative change - down syndrome, RA, os odontiodium
- sx:
- neck pain, neuro sx/deficits
- myelopathic sx: muscle weakness, hyperreflexia, wide gait, bladder dysfx
- dx:
- XRAY: ODOINTOID VIEW - may see inc in atlanto-dens interval
-tx: depends on cause
clay shoveler’s fracture
SPINOUS PROCESS AVULSION FRX MC AT LOWER CERVICAL (C6 OR C7) or upper thoracic vertebrae
-MOI: forced neck flexion w/ muscle pulling off piece of spinous process, esp after sudden deceleration injuries (mva); usually stable injury
- tx:
- NONOPERATIVE: nsaids, rest, immobilization in hard collar for comfort
- surgical excision only used if non-union or persistent pain
flexion teardrop fractures
ANTERIOR DISPLACEMENT OF A WEDGE-SHAPED FRACTURE FRAGMENT (teardrop shape of ANTERIO-INFERIOR PORTION of superior vertebra)
MOI: severe flexion and compression causes the vertebral body to collide w/ an inferior vertebral body
- mc in lower cervical spine; loss of vertebral height
- HIGHLY UNSTABLE (bc disrupts posterior longitudinal ligament) MAY CAUSE ANTERIOR CERVICAL CORD SYNDROME
-tx: SURGERY
extension teardop fractures
-triangular-shaped avulsion fracture of the antero-inferior corner of the vertebral body as a result of the rupture of the anterior longitudianl ligament
MOI: ABRUPT NECK EXTENSION
-MC SEEN AT C2, may be seen at C5-C7 and assoc w/ central cord syndrome, no loss of vertebral height
-tx: CERVICAL COLLAR
burst fractures
-d/t nucleus pulposus of intervertebral disc being forced into vertebral body, causing it to burst outwards
MOI: axial loading injury causing vertebral compression injures of the cervical and lumbar spine
Stable: all ligaments intact, no posterior displacement
Unstable: >50% copression of spinal cord, 50% loss of vertebral height, >20 degrees of spinal angulation or assoc neuro deficits
XRAY: comminuted vertebral body and loss of height
-tx: UNSTABLE NEEDS SURGICAL CORRECTION
subclavian steal syndrome
signs/sx from reversed blood flow down ipsilateral vertebral artery to supply affected arm d/t occlusion or stenosis of subclavian artery; L ARM MC AFFECTED
Etiologies: ATHEROSCLEROSIS MC, thoracic outlet synd
- sx:
- most asymptomatic
- SX OF ARM ARTERIAL INSUFFICIENCY: claudication, paresthesias, BLOOD PRESSURE DIFFERENCE BTW ARMS (reduction in affected arm >15 mmHg)
- SX OF VERTEBROBASILAR INSUFFICIENCY: presyncope/syncope, dizzy, neuro deficits, vertigo, diplopia, nystagmus, weak, drop attacks, gait
- dx:
- continuous-wave doppler, duplex US, transcranial doppler, ct angio
- tx:
- revascularization or percutaneous transluminal angio in severe
anterior cord syndrome
MOI:
- MC after blowout vertebral body burst fracture (flexion)
- anterior spinal artery injury or occlusion
- direct anterior cord compression
- aortic dissection, sle, aids
Deficits:
MOTOR: LOWER EXTREMITY > UPPER (corticospinal)
SENSORY: pain, temp (spinothalamic), light touch, may devo BLADDER DYSFUNCTION (incontinence, retention)
Preserved:
-proprioception, vibration, pressure (dorsal column spared)
central cord syndrome
MOI:
- hyperextension injures (50% w/ mva), falls in elderly, gsw, tumors, cervical spinal stenosis, syringomyelia
- MC incomplete cord syndrome
- it affects primarily the central gray matter
Deficits:
MOTOR: UPPER EXTREMITY > LOWER (distal portion more severe involvement from corticospinal involvement)
SENSORY: pain, temp (spinothalamic) deficit greater in upper extremity –> SHAWL DISTRIBUTION
Preserved:
-proprioception, vibration, pressure (dorsal column spared)
posterior cord syndrome
MOI: rare
-damage to posterior cord or posterior spinal stenosis
Deficits:
-LOSS OF PROPRIOCEPTION AND VIBRATORY ONLY
Preserved:
-pain, light touch; no motor deficits
brown sequard
MOI:
- unilateral hemisection of the spinal cord
- MC after PENETRATING TRAUMA, tumors
- rare
Deficits:
IPSILATERAL DEFICITS
-MOTOR: lateral corticospinal tract, VIBRATION AND PROPRIOCEPTION (dorsal column)
CONTRALATERAL DEFICITS
-PAIN AND TEMP (lateral spinothalamic tract) usually 2 levels below injury
anterior circulation ischemic stroke lesions
Right-sided Lesions
- bx, learning process, short-term memory
- left hemiparesis, sensory loss, neglect, ANOSOGNOSIA
- left homonymous hemianopsia, APRAXIA
- dysarthria, SPATIAL/TIME DEFICITS
- FLAT AFFECT, IMPAIRED JUDGEMENT, IMPULSIVITY
Left-sided Lesions:
- speech language
- right hemiparesis, sensory loss, homonymous hemianopsia, dysarthria
- APHASIA, AGRAPHIA, DEC MATH COMPREHENSION
terms
hemiparesis = weakness
hemiplegia = paralysis
dysarthria = inability to articulate words
apraxia = loss of ability to execute purposeful mvmts
ataxia = loss of coordinated mvmts
aphasia = difficulty remembering words, speaking, write
broca’s aphasia = frontal lobe nonfluency, sparse output (comprehension relatively preserved)
wernicke’s aphasia = fluent aphasia (volume, meaningless) w/ marked impaired comprehension
transient ischemic attack
- caused by focal brain, spinal cord or retinal ischemia WITHOUT ACUTE INFARCTION
- OFTEN LASTS <24 H (most resolve 30-60 m)
- MC DUE TO EMBOLUS or transient hypoTN
- 50% of pt will have CVA w/in 24-48 h after (esp DM, HTN) 10-20% will experience CVA w/in 90 days
-sx:
INTERNAL CAROTID:
-AMAUROSIS FUGAX (MONOCULAR VL - LAMP SHADE DOWN ONE EYE), WEAKNESS CONTRALATERAL HAND
-sudden ha, speech, changes, confusion
VERTEBROBASILAR
-BRAINSTEM/CEREBELLAR SYMPTOMS (gait, proprioception, dizzy, vertigo)
-dx:
-CT HEAD - INITIAL TEST OF CHOICE to r/o hemorrhage
-CAROTID DOPPLER - endarterectomy rec if internal or carotid stenosis 70+%
-CT ANGIO, MRI AGIO
-blood sugar to r/o hypoglycemia, r/o electrolyte issue, coag studies, cbc
-TTE or TEE to look for cardioembolic sources
-ECG to look for a-fib
ABCD2 score to assess CVA risk: Age, Bp, Clinical features, Duration of sx, Diabetes
- tx:
- ASA +/- CLOPIDOGREL OR DIPYRIDAMOLE
- THROMBOLYTICS CONTRAINDICATED!!!
- place supine to inc cerebral perfusion, avoid lowering bp
- reduce modifiable rf: DM (gluc control), HTN, A-fib
ischemic stroke
-MC 80% d/t TROMBOTIC 49%, EMBOLI 31%, cerebrovascular occlusion
- LACUNAR STROKE:
- SMALL VESSEL DZ atheroembolic stroke, penetrating arteries providing blood to the brain’s deep structures is occluded
- PURE MOTOR MC, ATAXIC HEMIPARESIS, DYSARTHRIA, HX OF HTN 80%
- CT: SMALL PUNCHED OUT HYPODENSE AREAS
- tx: ASA, control risk factors
MIDDLE CEREBRAL ARTERY - MC 70%
- contralateral sensory/motor loss/hemiparesis: GREATER IN FACE, ARM > leg/foot
- GAZE PREFERENCE TOWARDS SIDE OF LESION
- LEFT SIDE –> APHASIA: BROCA, WERNICKE, MATH COMPREHENSION, AGRAPHIA
- RIGHT SIDE –> SPATIAL DEFECTS, DYSARTHRIA, LEF-SIDE NEGLECT, ANOSOGNOSIA, APRAXIA
ANTERIOR CEREBRAL ARTERY
- contralateral sensory/motor loss/hemiparesis: GREATER IN LEG/FOOT –> ABN GAIT
- FACE SPARED, speech preserved, slow response
- frontal lobe and mental status impairment: IMPAIRED JUDGMENT, CONFUSION, PERSONALITY CHANGES (FLAT AFFECT)
- URINARY INCONTINENCE, upper motor neuron weak
- gaze pref towards side of lesion
POSTERIOR CEREBRAL ARTERY
-VISUAL HALLUCINATIONS, CONTRALATERAL HOMONYMOUS HEMIANOPSIA, “CROSSED SX” (ipsilateral cranial nerve deficits, contralateral muscle weakness), coma, drop attacks
BASILAR ARTERY
-cerebral dysfx, CN palsies, dec vision, dec bilateral sensory
VERTEBRAL ARTERY
-VERTIGO, NYSTAGMUS, N/V, DIPLOPIA, ipsilateral ataxia
- dx:
- NON-CONTRAST CT: r/o hemorrhage (may be normal first 6-24h)
- tx:
- THROMBOLYTICS W/IN 3 HOURS of onset
- ALTEPLASE (tissue plasminogen activator TPA) given if no evidence of hemorrhage (c/i BP >185/110, recent bleed/trauma, bleeding disorder)
- antiplatelet: asa, clopidogrel, dipyridamole, +/- anticoag if cardioembolic
- only lower BP if >185/110 for thrombolytics or >220/120 if no thrombolytic use
- STROKES W/ FACIAL INVOLVEMENT INVOLVES LOWER HALF OF FACE (WILL STILL BE ABLE TO RAISE EYEBROW)
hemorrhagic stroke
- 20% of strokes
- HA, VOMITING FAVORS ICH OR SAH
- IMPAIRED CONSCIOUSNESS W/OUT FOCAL SX FAVORS SAH
SPONTANEOUS ICH
- COMMONLY CAUSED BY HTN, esp BASAL GANGLIA
- LOC, n/v, hemiplegia, hemiparalysis
- sx usually min-hrs gradually increasing
- NONCONTRAST CT -don’t perform LP if ICH suspected!
- tx: supportive vs. hematoma evacuation; if inc intracranial pressure –> head elevation +/-mannitol, hyperventilation
SUBARACHNOID HEMORRHAGE
- SUDDEN, “WORST HA OF MY LIFE” –> BRIEF LOC, N/V, MENINGEAL IRRITATION, nuchal rigidity, seizures
- MC 2ry TO RUPTURE OF BERRY ANEURYSM or AVM
- no focal neurological sx
- CT SCAN –> if neg and high suspicion –> LP (XANTHOCHROMIA / RBC) esp if inc pressure
- tx: bedrest, no exertion/strain, anti-anxiety meds, stool softeners +/- lower BP
BERRY ANEURYSM
-MC CIRCLE OF WILLIS
-ANGIOGRAPHY GOLD STD
+/-ANEURYSM CLIP/COIL
epidural hematoma (hemorrhage)
Location:
ARTERIAL BLEED MC BTW SKULL AND DURA
Mechanism:
MC AFTER TEMPORAL BONE FRACTURE –> MIDDLE MENINGEAL ARTERY
- sx:
- varies, brief LOC –> lucid interval –> coma
- ha, n/v, focal neuro sx, rhinorrhea (csf)
- CN III palsy if tentorial herniation
- dx:
- CT: CONVEX (LENS-SHAPE) BLEED
- DOESNT CROSS SUTURE LINES
- tx:
- may herniate if not evacuated early, observe if small
- if INC ICP –> MANNITOL, hyperventilation, head elevation, shunt
subdural hematoma (hemorrhage)
Location:
VENOUS BLEED MC - btw dura and arachnoid d/t TEARING OF CORTICAL BRIDGING VEINS
-MC IN ELDERLY
Mechanism:
-MC BLUNT TRAUMA - often causes bleeding on other side of injury “CONTRE-COUP”
- sx:
- varies, may have focal neuro sx
- dx:
- CT: CONCAVE (CRESCENT-SHAPED) BLEED
- BLEEDING CAN CROSS SUTURE LINE
- tx:
- hematoma evac vs. supportive
- evac if massive or 5+mm midline shift
subarachnoid hemorrage (SAH)
Location:
ARTERIAL BLEED btw arachnoid and pia
Mechanism:
-MC BERRY ANEURYSM RUPTURE, AVM
-sx:
-THUNDERCLAP SUDDEN HA “WORSE HA OF LIFE”, +/- unilateral, occipital area
+/-LOC, n/v, MENINGEAL SX: STIFF NECK, PHOTOPHOBIA, DELIRIUM
-NO FOCAL NEURO DEFICITS
-TERSON SYNDROME: retinal hemorrhages
- dx:
- CT SCAN
- if negative CT –> LP: XANTHOCHROMIA (RBC), INC CSF PRESSURE
- 4-VESSEL ANGIO after confirmed SAH
-tx:
-supportive: bed rest, stool softeners, lower icp
-surgical coil/clip
+/- lower BP gradually (NICARDIPINE, NIMODIPINE, labetalol)
intracerebral hemorrhage (ICH)
Location:
INTRAPARENCHYMAL
Mechanism:
-HTN, trauma, amyloid, ArterioVenous Malformation (AVM)
- sx:
- HEADACHE, N/V, +/- LOC, hemiplegia, hemiparesis
- not assoc w/ lucid intervals
- dx:
- CT: intraparenchymal bleed
- DON’T PERFORM LP IF SUSPECTED BC MAY CAUSE BRAIN HERNIATION
-tx:
-supportive: gradual bp reduction
+/-MANNITOL IF INC ICP
+/-hematoma evac if mass effect
acute bacterial meningitis
-may have hx of sinusitis or pneumonia prior to devo of meningitis
-sx:
-FEVER/CHILLS (95%), MENINGEAL SX: ha, nuchal rigidity, photosensitivity, n/v –> AMS, SEIZURES
+KERNIG’S SIGN: inability to straighten knee w/ hip flexion
+BRUDZINSKI’S SIGN: neck flexion produces knee/hip flexion
-dx:
-LUMBAR PUNCTURE: CSF EXAMINATION DEFINITIVE
100-1000 PMN, DEC GLUCOSE (<45), INC TOTAL PROTEIN, INC CSF PRESSURE
-HEAD CT: to r/o mass effect BEFORE LP if high risk (>60, immunocomp, h/o CNS dz, AMS, focal neuro findings, papilledema)
- tx:
- DON’T WAIT FOR LP RESULTS - START EMPIRIC
<1 mo –> GROUP B STREP (STREP AGALACTIAE) MC
-AMP (listeria) + CEFOTAXIME
1 mo - 18y –> N. MENINGITIDIS MC (ASSOC PETECHIAL RASH)
-CEFTRIAXONE (CEFOTAXIME) + VANC
18y - 50y –> S. PNEUMO MC, N. MENINGITIDIS
-CEFTRIAXONE (CEFOTAXIME) + VANC
> 50y –> S. PNEUMO, LISTERIA
-AMP + CEFTRIAXONE (CEFOTAXIME) +/-VANC
*DEXAMETHASONE RECOMMENDED IF KNOWN/SUSPECTED S.PNEUMO
Prophylaxis/exposed: CIPRO 500mg x 1 dose, alternate Rifampin
viral (aseptic) meningitis
VIRAL INFX OF MENINGES
-ENTEROVIRUS FAMILY MC (echovirus, coxsackie), ARBOVIRUSES (transmitted by mosquitoes), mumps, HSV 1+2, HIV
-sx:
-ha, fever, mild confusion
+MENINGEAL SX: nuchal rigidity, +Brudzinski, +Kernig, photophobia, phonophobia, lethargy (sx not as intense as bacterial)
-ASSOC W/ NORMAL CEREBRAL FX - not asoc w/ neuro deficits or seizures
-dx:
-CT FIRST TO R/O MASS
-CSF ANALYSIS: MOST IMPORTANT TO DIFFERENTIATE
lymphocytosis, normal glucose, +/-inc protein
-MRI: diffuse enhancement of meninges; frontal/temporal seen w/ HSV-1
-serologies, viral cx
- tx:
- SUPPORTIVE: antipyretics, fluids, antiemetics
- good prognosis, usually self-limited (7-10d)
encephalitis
VIRAL INFX OF BRAIN PARENCHYMA
-HSV-1 MC CAUSE, Enteroviruses, Arboviruses, zoster, rubeola, toxoplasmosis, cmv, rabies
- sx:
- ha, fever, PROFOUND LETHARGY, AMS
- ASSOC W/ ABNORMAL CEREBRAL FX AND FOCAL NEURO DEFICITS (ex cranial nerve II, IV, VI, VII), sensory and motor deficits, personality, mvmt, speech and bx disorders, SEIZURES
- dx:
- CSF ANALYSIS: SAME AS VIRAL - LYMPHOCYTOSIS, NORMAL GLUCOSE, inc protein
- Brain Imaging: temporal lobe mc involved (+/- mass eff)
-tx:
-SUPPORTIVE: antipyretics, fluids, control cerebral edema, seizure prophylaxis if needed
-VALACYCLOVIR if HSV or no identifiable cause of meningitis (hsv assoc w/ poor prognosis)
+/-Immunoglobulin if immunocompromised
-assoc w/ higher M/M than viral; HSV assoc w/ 70% mortality if not treated
simple partial (focal) seizure
CONSCIOUSNESS FULLY MAINTAINED
EEG: focal discharge at onset of seizure
-may have focal sensory, autonomic, motor sx
-may be followed by transient neurologic deficit lasting up to 24 hrs
complex partial (focal - temporal lobe) seizure
CONSCIOUSNESS IMPAIRED, starts focally
EEG: interictal spikes w/ slow waves in temporal area
Aura (sec-min) –> impaired consciousness
- Auras: sensory/autonomic/motor sx of which the pt is aware; may precede/accompany or follow
- AUTOMATISMS: LIP SMACKING, MANUAL PICKING, PATTING, COORDINATED MOTOR MVMT
absence (petit mal) generalized seizure
BRIEF LAPSE OF CONSCIOUSNESS; pt usually unaware of attacks
BRIEF STARING EPISODES, EYELID TWITCHING
NO POST-ICTAL PHASE
-may be clonic (jerk), tonic (stiff) or atonic (loss of postural tone)
-MC IN CHILDHOOD –> USUALLY STOPS BY 20Y
EEG: bilateral symmetric 3Hz spike and wave action or normal
- tx:
- ETHOSUXIMIDE 1ST LINE (only works for absence), Valproic acid 2nd line
tonic-clonic (grand mal) generalized seizure
TONIC PHASE: LOSS OF CONSCIOUSNESS –> RIGID, sudden arrest of respiration (usually <60sec) –> clonic phase
CLONIC PHASE: REPETITIVE, RHYTHMIC JERKING (LASTS <2-3 MIN) –> postictal phase
POSTICTAL PHASE: FLACCID COMA / SLEEP (VARIABLE DURATION)
- may be accompanied by incontinence, tongue biting or aspiration w/ postictal confusion
- AURAS ARE PREWARNINGS TO SEIZURES
EEG: generalize high-amp rapid spiking, may be normal in between seizures
- tx:
- VALPROIC ACID, PHENYTOIN, CARBAMAZEPINE, LAMOTRIGINE, topiramate, primadone, levetiracetam, gabapentin, phenobarbital, midazolam
myoclonus (generalized)
SUDDEN, BRIEF, SPORADIC INVOLUNTARY TWITCHING, NO LOC
-maybe 1 muscle or group of muscles
- tx:
- Valproic Acid, Clonazapam
atonic (generalized)
“DROP ATTACKS” - SUDDEN LOSS OF POSTURAL TONE
status epilepticus (generalized)
repeated, generalized seizures w/out recovery >30 min
- tx:
- LORAZEPAM OR DIAZEPAM –> PEHNYTOIN –> PHENOBARBITAL
- thiamine + ampule of D50
- place left-lateral-decubitus position
differentiate btw pseudoseizures
prolactin levels increased in true seizures
