Glossary of Block VIII, Week III
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- 3 types of cerebral edema?
- describe vasogenic cerebral edema
- leakage of fluid from damaged microvasculature
- describe cytotoxic cerebral edema
- cellular injury with cytoplasmic swelling
- describe interstitial cerebral edema
- ventricular fluid diffuses into brain parenchyma
- major clinical complication/manifestation of cerebral edema -"bottom line"?
- may cause or contribute to increased intracranial pressure
- treatment for increased intracranial pressure?
- herniation may occur as a complication to increased intracranial pressure. order of herniation in top 4 locations?
- 1. cingulate (under edge of falx)
3. cerebellar tonsillar (through foramen magnum)
4. transcalvarial (through open skull defect)
- which vasculature structure is affected in a cingulate herniation?
- branches of the anterior cerebral artery (infarction)
- structures affected in an uncal/transtentorial herniation?
- oculomotor nerve
posterior cerebral a. (infarction)
aqueduct of sylvius (obstruction)
basilar perforating arteries
- clinical s/s of oculomotor nv. involvement seen in an uncal herniation?
- ipsilateral fixed, dilated pupil
- clinical s/s of posterior cerebral a. involvement in an uncal herniation?
- clinical s/s of cerebral peduncle involvement in an uncal herniation?
- pathological finding in basilar perforating arteries affected in uncal herniation?
- Duret hemorrhages seen in pons
- what structure is affected in a cerebellar tonsilar herniation?
- medulla, respiratory centers
(see depression of consciousness and respirations)
- CSF is produced where and resorbed where?
- produced in choroid plexus of lateral, fourth ventricles
resorbed in arachnoid granulations
- non-communicating hydrocephalus is usually the result of a blockage where?
- aqueduct or interventricular foramina
- four mechanisms of non-communicating hydrocephalus
- 1. congenital (stenosis)
2. neoplasm (ie. choroid plexus adenoma)
3. inflammation (ventriculitis, meningitis)
4. intraventricular hemorrhage
- what causes communicating hydrocephalus?
- impaired resorption of CSF at the arachnoid granulations (obstructive process involving the meninges)
- effects of the mass effect caused by an epidural hematoma?
- increased intracranial pressure -> get uncal/transtentorial herniation with associated neurological signs (ipsilateral fixed pupillary dilation)
- subdural hematoma is MC seen in what age group?
(cerebral atrophy predisposes to avulsion of bridging veins)
- what other group, besides the elderly, are at high risk for subdural hematomas?
- chronic alcoholics
- how might a subdural hematoma present in an elderly patient?
(DDx: AD, dementia)
- clinical s/s of an subarachnoid hemorrhage?
- *meningeal irritation (complain of worst H/A ever had)
*no pupillary symptoms (no mass effect)
*may see hyponatremia develop (due to SIADH)
- what is the MCC of an subarachnoid hemorrhage?
- spontaneous rupture of a berry aneurysm
- diffuse axonal injury is due to what mechanism?
- rotational/shearing forces within the brain
- clinical findings in diffuse axonal injury?
(do see decreased consciousness or coma)
- a congenital disorganized cluster of arteries and veins in the brain is called?
- arteriovenous malformation (AVM)
- are AVMs inherited or sporadic?
- clinical implications of an AVM?
- may act as a focus for seizures
may have episodic hemorrhage
- clinical implications of a cavernous hemangioma?
*most are asymptomatic and incidentally found
- clinical implications of capillary angiomas, venous angiomas, telangectasias?
most are asymptomatic, found incidentally
- berry aneurysms have an association with what disease?
- polycystic kidney disease
- what type of hemorrhage does a ruptured berry aneurysm lead to?
- subarachnoid hemorrhage
(35% mortality at time of 1st bleed)
- most berry aneurysms are found?
- in the anterior part of the circle of willis
- besides berry aneurysms: what 4 other types of aneurysms are there in the CNS?
- 1. atherosclerotic
- atherosclerotic aneurysms are MC found in which artery?
(may thrombose but do not rupture)
- what is the other name for hypertensive aneurysms?
- Charcot-Bouchard (microaneurysms of the arterioles)
- rupture of a hypertensive anuerysm results in what type of hemorrhage?
- what is a mycotic aneurysm?
- infective aneurysm (usually from septic amboli, ie. endocarditis)
- a traumatic vertebral artery dissection is also known as?
- pathogenesis of amyloid angiopathy
- amyloid deposited in small vessel walls, tendency to rupture. NOT DUE TO HTN
- three types of neurons that are extremely susceptible to ischemia?
- purkinje cells of cerebellum
neurons in basal ganglia
- what is the usual cause of small vessel disease leading to a stroke?
- chronic HTN
- what are some hematologic causes of stroke?
- prothrombotic states
(polycythemia vera, sickle cell disease, protein C, S, antithrombin deficiencies, leukemia, DIC)
- occlusion of perforating small arteries tends to cause what kind of infarct?
- lacunar infarct
(pure motor or sensory deficit)
- in regards to ischemia and infarction: a deficit that lasts <24 hrs is called?
transient ischemic attack
(usually lasts 5-30 min)
- in regards to ischemia and infarction: a deficit that lasts >24 hrs but <3 wks is called?
- reversible ischemic neurologic deficit
- in which type of infarct is it advised to "do nothing," as treatment will cause increased injury upon reperfusion?
- hemorrhagic infarct
- gross manifestations of a cerebral infarction at:
1. 6-12 hrs
2. 48-72 hrs
3. >72 hrs
- 1. mild softening, blurring of grey-white matter junction
2. marked softening and edema
3. coagulation necrosis, eventual cavitation
- micro manifestations of a cerebral infarction at:
1. 12-24 hrs
2. >24 hrs
- 1. red dead neurons
2. influx of neutrophils and macrophages
3. peripheral gliosis, central cavitation
- describe injury to the peripheral axon
- *focal (trauma) or generalized (DM) injury
*wallerian degeneration of axons distal to injury
*may have chromatolysis of neuron cell body
*secondary disintigration of myelin sheath
- describe myelin (Schwann cell) injury
- *segmental myelin sheath damage, with segmental cells present
*underlying axon intact, potential for remyelination
- what is the MCC of peripheral neuropathy worldwide?
- is Guillan-Barre more common in males or females?
- describe the clinical s/s of guillan-barre
- acute onset of rapidly progressing motor, sensory and autonomic disturbances
*LMN disturbances (symmetrical weakness, hyporeflexia)
- what is the pathogenesis of guillan-barre?
- immune mediated disease
*lymphocytic infiltrates around peripheral nerves
*schwann cell injury, peripheral demyelination
- in guillan-barre - approx. 1/3 have a history of illness 2-3 wks prior. what types of illness did they commonly have?
- 1. upper respiratory infx (ie. mycoplasma)
2. GI (ie. campylobacter jejuni)
*also have been associated with vaccinations, lymphomas, some drugs, pregnancy
- CSF studies seen in Guillan-Barre?
- elevated protein
- clinical course of G-B?
- usually self-limited
Tx. is supportive
- what is the equivalent of "MS" in the PNS?
- chronic inflammatory demyelinating polyradiculoneuropathy
- treatment for chronic inflammatory demyelinating polyradiculoneuropathy?
- what are the 3 types of neuropathy seen in DM?
- 1. diffuse symmetric axonal injury (MC)
2. mononeuropathy or plexopathy
3. autonomic neuropathy (symp/parasymp)
- clinical manifestations of autonomic neuropathy seen in DM?
*GI (stomach, bowel motility dysfx)
*GU (bladder, erectile dysfx)
- carpal tunnel injury is due to damage to which nerve?
- saturday night palsy is due to damage of which nerve?
- radial nerve
- what is a traumatic neuroma?
- disorganized attempt at nerve regeneration, often at sites of major or minor nerve transection, may be painful
- histology seen in a traumatic neuroma?
- sprouting axons
proliferating schwann cells
- clinical s/s of Morton's neuroma?
- shooting pain around ball of foot
pain worse with weightbearing
- histology seen in Morton's neuroma?
- perineural fibrosis
- which tumor of the PNS characteristically has palisading nuclei upon histological examination?
- where are neurofibromas MC seen?
- what do neurofibromas consist of?
- disorganized schwann cells
- what is the plexiform type of neurofibroma and what is significant about it?
- involves peripheral nerves
*when present is pathognnomonic for neurofibromatosis type I*
- what is the basic difference between a schwannoma and a neurofibroma?
- schwannoma - no neural infiltration
neurofibroma - expand whole nerve, within nerve
- what are the only two situations in which a malignant peripheral nerve sheath tumor asrises?
- 1. neurofibromatosis (neurofibroma turned malignant)
2. large nerve trunk
- inheritance pattern of neurofibromatosis?
- where is the mutation found in neurofibromatosis type I?
- chromosome 17
- three characteristics of NF type I?
- 1. cafe-au-lait spots
2. multiple cutaneous neurofibromas
3. Lisch nodules - pigmented iris hamartomas
- where is the mutation found in NF type II?
- chromosome 22
- 4 characteristics of NF type II?
- 1. bilateral acoustic neuromas
- inheritance pattern of tuberous sclerosis?
- in relation to tuberous sclerosis - pathologic findings in:
- 1. hamartomas
2. ash-leaf patches (hypopigmented areas), angiofibromas of face (adenoma sebaceum)
3. rhabdomyomas of heart, angiomyolipomas of kidney, cysts in liver, kidney, pancreas
- transmission of von-hippel lindau syndrome?
- where is the mutation found in von-hippel-lindau?
- chromosome 3
- in relation to von-hippel-lindau syndrome: pathologic features in:
- 1. cerebellar hemangioblastomas
2. retinal angiomas
3. cysts in liver, kidneys, pancreas, angiomas
- von-hippel-lindau syndrome is associated with an increased risk of what cancer?
- renal cell carcinoma
- manifestations of sturge-weber syndrome in the brain?
- ipsilateral leptomeningial angiomas with underlying atrophy of cerebral cortex
- what is the composition of prions?
- NO NUCLEIC ACID COMPONENT
- are prions hardy or not?
- very hardy
can be exposed to heat, radiationand chemical disinfectants and still survive
- prognosis of a prion disease once symptoms appear?
- NO remission or recovery
- four prion diseases seen in humans?
- 1. Kuru
3. gerstmann-straussler-scheinker syndrome (GSS)
4. fatal familial insomnia (FFI)
- describe the prion hypothesis
- PrPsc (prion protein)forms beta sheets and is protease resistant. it serves as a template for converting normal protein into PrPsc. this modification is permanent
- why are animal forms of prion diseases inefficiently transmitted to humans?
- species barrier
- where do prions replicate in the human host?
- lymphoid tissues and spleen
- what (in regards to the immune system) is required for prions to enter the CNS?
- a competent immune system with fully differentiated B cells
- characteristic histo findings in spongiform encephalopathies?
- *vacuolation of dendritic and axonal processes
*proliferation and hypertrophy of astrocytes
*spongiform gray matter
*amyloid plaques and fibrils
- age of onset of CJD?
- 40-70 yrs
- is CJD familial or sporadic?
(most sporadic (85%), some familial)
- incubation time of "infectious" CJD?
- 3-20 yrs
- 3 MC s/s seen in CJD?
- dementia (seen in all)
- inheritance of gerstmann-strassler-scheinker syndrome?
- compare the clinical s/s of gerstmann-strassler-scheinker syndrome to CJD
- gerstmann-strassler-scheinker syndrome - like CJD, but cerebellar ataxia is dominant feature
- inheritance pattern of fatal familial insomnia (FFI)?
- what is the predominant clinical feature of FFI?
- progressive insomnia
- shape of the rabies virus?
- bullet shaped
- describe the genome of the rabies virus
- the rabies virus genome only encodes how many genes?
- what is the protein found in the envelope that targets neutralizing antibodies called?
- G protein
- three hosts of rabies in the US?
- transmission of rabies virus?
- *virus-containing saliva inoculation through broken skin
- behavioral patterns seen in animals infected with the rabies virus?
more likely to attack unprovoked
- what causes the hydrophobia seen in rabies patients?
- spasms of the muscles of deglutition - inability to drink or swallow saliva
- what is the mortality rate of rabies once prodromal symptoms have appeared?
- diagnosis of rabies?
- fluorescent antibody staining of skin biopsy or hair follicles
- classic histo of rabies infection?
- Negri bodies (eosinophilic inclusions in brain tissue)
- how is post-exposure rabies treated?
- brain tumors MC arise from which cell type?
- glial cells
- are most astrocytomas benign or malignant?
- astrocytomas tend to involve which brain locations in:
- 1. cerebral hemospheres
2. posterior fossa, optic nerve
- in a high grade astrocytoma, what is the classic lesion seen on CT
- ring-enhancement lesion
- pilocytic astrocytomas are MC seen in what age group?
- MC location of a pilocytic astrocytoma?
(circumscribed cystic lesion with a mural nodule)
- behavior of a pilocytic astrocytoma?
- relatively benign
- where are oligodendrogliomas MC found?
- white matter of cerebral hemispheres
- common presentation of pts with oligodendrogliomas?
- compare the prognosis of an astrocytoma and an oligodendroglioma?
- oligodendroglioma has better prognosis (slower growing)
- what is seen upon a CT scan of an oligodendroglioma?
- what neoplasm is slow growing, circumscribed, MC seen in children, and MC occurs in the 4th ventricle or spinal cord?
- is an ependymoma MC benign or malignant?
- where are choroid plexus tumors MC located?
- in lateral or 4th ventricles
(where choroid plexus is)
- choroid plexus tumors are MC in which age group?
- what is the MC type of choroid plexus tumor?
- papillomas (benign)
- which CNS neoplasm is one of the "small blue cell tumors of childhood" and is commonly located in the cerebellum?
- what does the prognosis of a medulloblastoma depend on?
- extent of surgical resection
N-myc and C-myc oncogene amplification
- where do medulloblastomas tend to metastasize to?
- spinal cord
- describe the "character" of a meningioma
- indolent, most grow slowly
- where are meningiomas MC found
- intracranial or spinal location
- any connection between meningiomas and pregnancy?
- meningiomas may have estrogen receptors, therefore may grow more rapidly in pregnancy
- what is the classic growth pattern seen in a meningioma?
- whorling growth pattern
(also see psammoma bodies)
- where do most acoustic neuromas occur?
- involve CN VIII at the CEREBELLOPONTINE ANGLE
- bilateral acoustic neuromas should make you think of?
- neurofibromatosis type II
- where are most cranioparyngiomas located?
- suprasellar, in hypothalamic region
- germ cell neoplasms MC occur in which sex and age group?
- young men
- name four germ cell neoplasms commonly seen in the CNS?
- where do CNS hemangiomas MC occur?
- cerebellum, spinal cord
- syndrome with hereditary form of CNS hemangioma?
- von-hippel-lindau syndrome
- typical sites of origin of metastatic tumors to the brain?
- what are the 3 states of existence (according to the sleep lecturer)?
- what wave activity is seen in wakefullness?
- alpha waves
(restful wakefullness when eyes are closed)
*Alpha for Awake*
- describe stage I N-REM sleep
- *decreased alpha waves to <50%
*slow rolling eye mvmt
*decreased muscle tone
- describe stage II N-REM sleep
- *K complex
*no eye mvmt
- what type of waves are seen in stage 3 and 4 N-REM sleep?
- delta waves
- delta waves signify what kind of sleep?
- deep sleep "D for Deep Sleep"
(wake up from this and have foggy haze, poor judgement, poor memory)
- in which type of sleep is HR and RR irregular?
- in which type of sleep is skeletal muscle tone absent?
- in which type of sleep is penile tumescence and vaginal engorgement seen?
- in which stage of sleep is poikilothermia observed?
(that's why see sweating and chills in REM sleep)
- in what type of sleep do most sleep problems occur?
- REM sleep
- what are the 3 mechanisms underlying wakefullness and sleep?
- 1. circadian
- which type of sleep waves are important in cognitive maturation?
- delta waves
- where in the brain is REM sleep initiated?
- when are PGO waves seen?
- REM sleep only
- which 3 neurotransmitters have been shown to turn off REM?
- connection between adenosine and sleep?
- adenosine = sleep factor
- three aspects in the mechanism of N-REM sleep?
- 1. inhibiting process of cortex and thalamus
2. decreased excitability of cortex and hypothalamus (thalamic gating)
3. dissappearance of FFWs (fast freq. wavelets)
- what is thalamic gating?
- shutting off of excitability coming from the lower brain centers
- describe the effects of N-REM sleep on the following:
3. cerebral flow, metabolic rate
- 1. decreases
*remember: N-REM is primarily a PARASYMPATHETIC state*
- describe CO early in the morning
(that's why more MIs occur in the morning)
- what happens to the upper airway muscles in REM?
this increases airway resistance (see snoring and OSA)
- what else relaxes airway muscles?
- when are ACTH and cortisol levels highest?
- 4-8 am
- when is GH released?
- 90 minutes after sleep onset
- TSH and Melatonin release are circadian related. what does this mean?
- both are released in the evening and levels are lower in the daytime
- what is meant when it is said that PRL is sleep related?
- levels are increased in sleep, decreased in wakefulness
- any connection between gastric secretions and sleep?
- increased gastric secretions during sleep
- when is brain activity highest?
- REM > wake > nREM
- what is the correlation between age and quality of sleep?
- increase age, increase sleep complaints
- define parasomnias
- undesirable phsyical or experiential phenomena which occur exclusively during the sleep period or are exacerbated by sleep
- top 2 reasons for excessive daytime sleepiness?
- 1. apnea
2. insufficient sleep
- historical term for sleep apnea?
- pickwickian syndrome
(70% of pts with OSA are overweight)
- symptoms of OSA?
- excessive sleepiness
choking or gasping in sleep
- predisposing factors to OSA?
- Age (40-60yrs)
- CV complications of OSA?
pulmonary HTN, cor pulmonale
brady or tachycardia
complete heart block
- possible therapies for OSA?
- 1. positive airway pressure
2. oral appliances
- s/s of narcolepsy
- 1. excessive daytime sleepiness
2. cataplexy (REM intrusion on the state of wakefullness)
- when is cataplexy MC seen?
- strong emotion
(bilateral loss of muscle tone provoked by strong emotion)
- what are hypagognic hallucinations?
- vivid, frightening, dream like experiences that occur in the transition from wakefullness to sleep or vice versa
- describe the nocturnal sleep habits of a pt with narcolepsy
- disturbed nocturnal sleep
(sleep fragmentation, nightmares, hypnagogic hallucinations, sleep paralysis, sleep apnea)
- human narcolepsy shows a loss of what neurgenic substance?
- what is the normal requirement for sleep?
- ranges from 4-10 hrs
- what are some medical conditions that can cause insomnia?
- what is psychophysiological insomnia?
- conditioned arousal to sleep environment
- what is delayed sleep phase syndrome?
- can't fall asleep until 2-3 am, wake up at 7 or 8am. whole wake/sleep cycle is shifted
- 3 MC parasomnias?
- 1. disorders of arousal
2. nocturnal seizures
3. REM sleep bahavior disorder
- 3 disorders of arousal?
- 1. confusional arousals
3. sleep terrors
- what are confusional arousals?
- confusion following arousal from sleep, disorientation
- what is REM sleep behavior disorder?
- abnormal intrusion of muscle tone in sleep, can be violent
(dreams acted out)
- what is the MC life threatening neurologic disease adn the 3rd leading cause of death in the USA?
- what is the difference between cerebral ischemia and a cerebral infarct?
- a cerebral infarct is dead neurologic tissue secondary to cerebral ischemia.
- how long after lack of blood flow does metabolic failure of cerebral tissue occur?
- 10 sec
(ie. if sudden anoxia such as choking or heart stops -> 10 sec. until unconscious)
- how long after lack of blood flow does irreversible damage of cerebral tissue occur?
- 4 minutes
- infarcted tissue is replaced with cystic areas. this is called?
- encephalomalacia (lack of brain tissue)
- what is the amount of blood flow to normal brain tissue?
- 50 mL/100g/min
- blood flow in an ischemic penumbra?
- <25 mL/100g/min
- cell death occurs at what blood flow?
- <10 mL/100g/min
- 84% of all strokes are of this type?
- three mechanisms of ischemic stroke?
- 1. large vessel
3. small vessel
- 2 mechanisms of hemorrhagic stroke?
- 1. vascular malformation
2. small vessel
- 3 vascular malformations that may result in a hemorrhagic stroke?
- 1. aneurysm
3. cavernous hemangioma
- at what size are saccular (berry) aneurysms mor elikely to rupture?
- >10 mm
- which sex, age is rupture of berry aneurysms MC in?
avg. age of rupture - 50 yrs
- rupture of a berry aneurysm results in what type of hemorrhage?
- "hypertensive hemorrhage" is due to rupture of?
- small vessels
(may cause lobar hemorrhage)
- top 3 locations of large vessel disease leading to ischemic stroke?
- 1. internal carotid
2. vertebral-basilar embolism
3. aortic arch
- what is the MCC of cardioembolic stroke?
- atrial fibrillation
- other causes of cardioembolic stroke?
- wall motion abnormalities
- what is the spectrum of small vessel ischemic disease?
- mild - gliosis, demyelination
moderate - lacunar stroke
severe - hypertensive hemorrhages, lobar hemorrhages
- prognosis of lacunar strokes compared to other forms of strokes?
(many recover function)
- which type os hemorrhage is caused by arterial degeneration with amyloid deposits in arterial walls?
- lobar intracerebral hemorrhage
- MC location of lobar intracerebral hemorrhage?
- cortical-subcortical junction
- some risk factors for ischemic stroke?
coronary artery disease
carotid artery disease
- hematologic and cellular disoroders that predispose to stroke?
- sickle cell
cardiolipin antibodies, lupus anticoagulants
protein C,S, antithrombin III deficiency
- s/s of an intracerebral hemorrhage?
- *acute onset neurologic deficit
*altered level of consciousness
*markedly elevated BP
- s/s of subarachnoid hemorrhage?
- *acute onet of severe H/A ("worst H/A of my life)
*confusion, LOC, seizures
*may progress and have focal neurologic signs
- describe the level of consciousness in an ischemic stroke
(unless bilateral brainstem reticular activating system is involved)
- symptoms of an anterior circulation stroke in the right (non-dominant) side?
- *L body weakness, numbness
*visual spacial neglect
*L hemifield loss
*amaurosis fugax (blindness in ipsilateral eye)
- symptoms of an anterior circulation stroke in the left (dominant) side?
- *R body weakness, numbness
*R hemifield loss
- symptoms of a stroke to the posterior circulation (brainstem)?
- dysarthria, dysphagia, diplopia, nystagmus, vertigo, mixed weakness/numbness, N/V, somnolence
- symptoms of a stroke to the posterior circulation (cerebellum)?
- symptoms of a stroke to the posterior circulation (occipital lobe)?
- hemifield visual defect
- symptoms of a stroke to the posterior circulation (medial temporal lobe)?
- give examples of some things that mimic TIAs
transient global amnesia
- in a young patient with a cryptogenic stroke, what should we be looking for?
- vascular abnormality or hypercoagulable state
- in which imaging modality (CT or MRI) does stroke show up earliest?
- which imaging modality is better to see hemorrhage with?
- which imaging modality shows blood flow in vessels?
- secondary prevention in a cardioembolic stroke?
- secondary prevention in a large vessel stroke?
- carotid endarterectomy
- secondary prevention in a small vessel stroke?
- risk factor management
- a cortical stroke is caused by?
- emboli from heart or large vessels
- a subcortical stroke is caused by?
- small vessel disease
- signs of a subcortical (small vessel) stroke?
- profound sensory or motor loss without aphasia or neglect
(cortical strokes have aphasia and neglect)
- most improvement after a stroke is in which timeframe?
- 1-3 months afterwards
(then slows down - will see most recovery by 2 yrs)
- which has a worse prognosis: intracerebral hemorrhage or subarachnoid hemorrhage?
- subarachnoid hemorrhage (mortality near 50%)
- acute treatment of ischemic strokes (medications)?
- secondary prevention of ischemic strokes?
- antiplatelet agent
control of BP, glucose and lipids
- why is reactive HTN allowed to go oup to 220/120 in ischemic stroke?
- want to keep penumbra alive
- treatment of hemorrhagic stroke?
- *correct blood clotting abnormalities
*only allow BP up to 140-180
- BP guidelines in a SAH?
- keep BP at normotensive range until aneurysm is clipped, then allow HTN and vascular expansion
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