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280 Cards in this Set
- Front
- Back
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3 types of cerebral edema?
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vasogenic
cytotoxic interstitial |
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describe vasogenic cerebral edema
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leakage of fluid from damaged microvasculature
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describe cytotoxic cerebral edema
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cellular injury with cytoplasmic swelling
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describe interstitial cerebral edema
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ventricular fluid diffuses into brain parenchyma
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major clinical complication/manifestation of cerebral edema -"bottom line"?
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may cause or contribute to increased intracranial pressure
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treatment for increased intracranial pressure?
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hyperventilation
O2 IV mannitol corticosteroids |
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herniation may occur as a complication to increased intracranial pressure. order of herniation in top 4 locations?
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1. cingulate (under edge of falx)
2. uncal/transtentorial 3. cerebellar tonsillar (through foramen magnum) 4. transcalvarial (through open skull defect) |
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which vasculature structure is affected in a cingulate herniation?
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branches of the anterior cerebral artery (infarction)
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structures affected in an uncal/transtentorial herniation?
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oculomotor nerve
posterior cerebral a. (infarction) cerebral peduncle aqueduct of sylvius (obstruction) basilar perforating arteries |
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clinical s/s of oculomotor nv. involvement seen in an uncal herniation?
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ipsilateral fixed, dilated pupil
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clinical s/s of posterior cerebral a. involvement in an uncal herniation?
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infarction
cortical blindness |
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clinical s/s of cerebral peduncle involvement in an uncal herniation?
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hemiplegia
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pathological finding in basilar perforating arteries affected in uncal herniation?
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Duret hemorrhages seen in pons
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what structure is affected in a cerebellar tonsilar herniation?
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medulla, respiratory centers
(see depression of consciousness and respirations) |
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CSF is produced where and resorbed where?
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produced in choroid plexus of lateral, fourth ventricles
resorbed in arachnoid granulations |
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non-communicating hydrocephalus is usually the result of a blockage where?
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aqueduct or interventricular foramina
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four mechanisms of non-communicating hydrocephalus
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1. congenital (stenosis)
2. neoplasm (ie. choroid plexus adenoma) 3. inflammation (ventriculitis, meningitis) 4. intraventricular hemorrhage |
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what causes communicating hydrocephalus?
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impaired resorption of CSF at the arachnoid granulations (obstructive process involving the meninges)
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effects of the mass effect caused by an epidural hematoma?
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increased intracranial pressure -> get uncal/transtentorial herniation with associated neurological signs (ipsilateral fixed pupillary dilation)
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subdural hematoma is MC seen in what age group?
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elderly
(cerebral atrophy predisposes to avulsion of bridging veins) |
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what other group, besides the elderly, are at high risk for subdural hematomas?
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chronic alcoholics
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how might a subdural hematoma present in an elderly patient?
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confusion
(DDx: AD, dementia) |
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clinical s/s of an subarachnoid hemorrhage?
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*meningeal irritation (complain of worst H/A ever had)
*no pupillary symptoms (no mass effect) *may see hyponatremia develop (due to SIADH) |
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what is the MCC of an subarachnoid hemorrhage?
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spontaneous rupture of a berry aneurysm
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diffuse axonal injury is due to what mechanism?
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rotational/shearing forces within the brain
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clinical findings in diffuse axonal injury?
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nonspecific
(do see decreased consciousness or coma) |
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a congenital disorganized cluster of arteries and veins in the brain is called?
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arteriovenous malformation (AVM)
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are AVMs inherited or sporadic?
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sporadic
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clinical implications of an AVM?
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may act as a focus for seizures
may have episodic hemorrhage |
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clinical implications of a cavernous hemangioma?
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NONE
*most are asymptomatic and incidentally found |
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clinical implications of capillary angiomas, venous angiomas, telangectasias?
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NONE
most are asymptomatic, found incidentally |
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berry aneurysms have an association with what disease?
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polycystic kidney disease
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what type of hemorrhage does a ruptured berry aneurysm lead to?
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subarachnoid hemorrhage
(35% mortality at time of 1st bleed) |
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most berry aneurysms are found?
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in the anterior part of the circle of willis
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besides berry aneurysms: what 4 other types of aneurysms are there in the CNS?
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1. atherosclerotic
2. hypertensive 3. mycotic 4. traumatic |
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atherosclerotic aneurysms are MC found in which artery?
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basilar
(may thrombose but do not rupture) |
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what is the other name for hypertensive aneurysms?
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Charcot-Bouchard (microaneurysms of the arterioles)
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rupture of a hypertensive anuerysm results in what type of hemorrhage?
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intracerebral
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what is a mycotic aneurysm?
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infective aneurysm (usually from septic amboli, ie. endocarditis)
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a traumatic vertebral artery dissection is also known as?
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pseudoaneurysm
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pathogenesis of amyloid angiopathy
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amyloid deposited in small vessel walls, tendency to rupture. NOT DUE TO HTN
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three types of neurons that are extremely susceptible to ischemia?
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purkinje cells of cerebellum
hippocampal neurons neurons in basal ganglia |
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what is the usual cause of small vessel disease leading to a stroke?
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chronic HTN
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what are some hematologic causes of stroke?
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prothrombotic states
(polycythemia vera, sickle cell disease, protein C, S, antithrombin deficiencies, leukemia, DIC) |
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occlusion of perforating small arteries tends to cause what kind of infarct?
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lacunar infarct
(pure motor or sensory deficit) |
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in regards to ischemia and infarction: a deficit that lasts <24 hrs is called?
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TIA
transient ischemic attack (usually lasts 5-30 min) |
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in regards to ischemia and infarction: a deficit that lasts >24 hrs but <3 wks is called?
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reversible ischemic neurologic deficit
(RIND) |
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in which type of infarct is it advised to "do nothing," as treatment will cause increased injury upon reperfusion?
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hemorrhagic infarct
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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 |
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micro manifestations of a cerebral infarction at:
1. 12-24 hrs 2. >24 hrs 3. later |
1. red dead neurons
2. influx of neutrophils and macrophages 3. peripheral gliosis, central cavitation |
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describe injury to the peripheral axon
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*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 |
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describe myelin (Schwann cell) injury
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*segmental myelin sheath damage, with segmental cells present
*underlying axon intact, potential for remyelination |
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what is the MCC of peripheral neuropathy worldwide?
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leprosy
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is Guillan-Barre more common in males or females?
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males
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describe the clinical s/s of guillan-barre
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acute onset of rapidly progressing motor, sensory and autonomic disturbances
*LMN disturbances (symmetrical weakness, hyporeflexia) *parasthesias |
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what is the pathogenesis of guillan-barre?
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immune mediated disease
*lymphocytic infiltrates around peripheral nerves *schwann cell injury, peripheral demyelination |
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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 |
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CSF studies seen in Guillan-Barre?
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elevated protein
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clinical course of G-B?
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usually self-limited
complete recovery Tx. is supportive |
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what is the equivalent of "MS" in the PNS?
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chronic inflammatory demyelinating polyradiculoneuropathy
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treatment for chronic inflammatory demyelinating polyradiculoneuropathy?
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prednisone
plasma xchange IVIg |
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what are the 3 types of neuropathy seen in DM?
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1. diffuse symmetric axonal injury (MC)
2. mononeuropathy or plexopathy 3. autonomic neuropathy (symp/parasymp) |
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clinical manifestations of autonomic neuropathy seen in DM?
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*cardiac
*GI (stomach, bowel motility dysfx) *GU (bladder, erectile dysfx) |
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carpal tunnel injury is due to damage to which nerve?
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median
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saturday night palsy is due to damage of which nerve?
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radial nerve
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what is a traumatic neuroma?
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disorganized attempt at nerve regeneration, often at sites of major or minor nerve transection, may be painful
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histology seen in a traumatic neuroma?
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sprouting axons
proliferating schwann cells |
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clinical s/s of Morton's neuroma?
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shooting pain around ball of foot
pain worse with weightbearing |
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histology seen in Morton's neuroma?
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perineural fibrosis
vascular microthrombi |
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which tumor of the PNS characteristically has palisading nuclei upon histological examination?
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schwannoma
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where are neurofibromas MC seen?
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skin
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what do neurofibromas consist of?
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disorganized schwann cells
mucous material collagen |
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what is the plexiform type of neurofibroma and what is significant about it?
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involves peripheral nerves
*when present is pathognnomonic for neurofibromatosis type I* |
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what is the basic difference between a schwannoma and a neurofibroma?
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schwannoma - no neural infiltration
neurofibroma - expand whole nerve, within nerve |
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what are the only two situations in which a malignant peripheral nerve sheath tumor asrises?
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1. neurofibromatosis (neurofibroma turned malignant)
2. large nerve trunk |
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inheritance pattern of neurofibromatosis?
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AD
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where is the mutation found in neurofibromatosis type I?
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chromosome 17
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three characteristics of NF type I?
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1. cafe-au-lait spots
2. multiple cutaneous neurofibromas 3. Lisch nodules - pigmented iris hamartomas |
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where is the mutation found in NF type II?
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chromosome 22
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4 characteristics of NF type II?
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1. bilateral acoustic neuromas
2. gliomas 3. meningiomas 4. neurilemmomas |
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inheritance pattern of tuberous sclerosis?
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AD
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in relation to tuberous sclerosis - pathologic findings in:
1. brain 2. skin 3. viscera |
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 |
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transmission of von-hippel lindau syndrome?
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AD
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where is the mutation found in von-hippel-lindau?
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chromosome 3
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in relation to von-hippel-lindau syndrome: pathologic features in:
1. brain 2. eyes 3. viscera |
1. cerebellar hemangioblastomas
2. retinal angiomas 3. cysts in liver, kidneys, pancreas, angiomas |
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von-hippel-lindau syndrome is associated with an increased risk of what cancer?
|
renal cell carcinoma
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manifestations of sturge-weber syndrome in the brain?
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ipsilateral leptomeningial angiomas with underlying atrophy of cerebral cortex
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what is the composition of prions?
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NO NUCLEIC ACID COMPONENT
just protein |
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are prions hardy or not?
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very hardy
can be exposed to heat, radiationand chemical disinfectants and still survive |
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prognosis of a prion disease once symptoms appear?
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NO remission or recovery
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four prion diseases seen in humans?
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1. Kuru
2. CJD 3. gerstmann-straussler-scheinker syndrome (GSS) 4. fatal familial insomnia (FFI) |
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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
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why are animal forms of prion diseases inefficiently transmitted to humans?
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species barrier
|
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where do prions replicate in the human host?
|
lymphoid tissues and spleen
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what (in regards to the immune system) is required for prions to enter the CNS?
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a competent immune system with fully differentiated B cells
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characteristic histo findings in spongiform encephalopathies?
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*vacuolation of dendritic and axonal processes
*proliferation and hypertrophy of astrocytes *spongiform gray matter *amyloid plaques and fibrils |
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age of onset of CJD?
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40-70 yrs
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is CJD familial or sporadic?
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both
(most sporadic (85%), some familial) |
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incubation time of "infectious" CJD?
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3-20 yrs
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3 MC s/s seen in CJD?
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dementia (seen in all)
involuntary mvmts cerebellar ataxia |
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inheritance of gerstmann-strassler-scheinker syndrome?
|
AD
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compare the clinical s/s of gerstmann-strassler-scheinker syndrome to CJD
|
gerstmann-strassler-scheinker syndrome - like CJD, but cerebellar ataxia is dominant feature
|
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inheritance pattern of fatal familial insomnia (FFI)?
|
AD
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what is the predominant clinical feature of FFI?
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progressive insomnia
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shape of the rabies virus?
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bullet shaped
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describe the genome of the rabies virus
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(-)ssRNA
enveloped |
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the rabies virus genome only encodes how many genes?
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5
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what is the protein found in the envelope that targets neutralizing antibodies called?
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G protein
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three hosts of rabies in the US?
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bats
skunks raccoons |
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transmission of rabies virus?
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*virus-containing saliva inoculation through broken skin
*infected aerosols |
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behavioral patterns seen in animals infected with the rabies virus?
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deranged
more aggressive more likely to attack unprovoked |
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what causes the hydrophobia seen in rabies patients?
|
spasms of the muscles of deglutition - inability to drink or swallow saliva
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what is the mortality rate of rabies once prodromal symptoms have appeared?
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>99%
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diagnosis of rabies?
|
fluorescent antibody staining of skin biopsy or hair follicles
|
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classic histo of rabies infection?
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Negri bodies (eosinophilic inclusions in brain tissue)
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how is post-exposure rabies treated?
|
vaccine
hyperimmune globulin |
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brain tumors MC arise from which cell type?
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glial cells
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are most astrocytomas benign or malignant?
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malignant
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astrocytomas tend to involve which brain locations in:
1. adults 2. children |
1. cerebral hemospheres
2. posterior fossa, optic nerve |
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in a high grade astrocytoma, what is the classic lesion seen on CT
|
ring-enhancement lesion
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pilocytic astrocytomas are MC seen in what age group?
|
children
|
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MC location of a pilocytic astrocytoma?
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intracerebellar
(circumscribed cystic lesion with a mural nodule) |
|
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behavior of a pilocytic astrocytoma?
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relatively benign
|
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where are oligodendrogliomas MC found?
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white matter of cerebral hemispheres
|
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common presentation of pts with oligodendrogliomas?
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seizures
|
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compare the prognosis of an astrocytoma and an oligodendroglioma?
|
oligodendroglioma has better prognosis (slower growing)
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what is seen upon a CT scan of an oligodendroglioma?
|
calcifications
|
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what neoplasm is slow growing, circumscribed, MC seen in children, and MC occurs in the 4th ventricle or spinal cord?
|
ependymoma
|
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is an ependymoma MC benign or malignant?
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benign
|
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where are choroid plexus tumors MC located?
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in lateral or 4th ventricles
(where choroid plexus is) |
|
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choroid plexus tumors are MC in which age group?
|
children
|
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what is the MC type of choroid plexus tumor?
|
papillomas (benign)
|
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which CNS neoplasm is one of the "small blue cell tumors of childhood" and is commonly located in the cerebellum?
|
medulloblastoma
|
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what does the prognosis of a medulloblastoma depend on?
|
extent of surgical resection
N-myc and C-myc oncogene amplification C-erb-B2 overexpression |
|
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where do medulloblastomas tend to metastasize to?
|
spinal cord
|
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describe the "character" of a meningioma
|
indolent, most grow slowly
|
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where are meningiomas MC found
|
intracranial or spinal location
|
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any connection between meningiomas and pregnancy?
|
meningiomas may have estrogen receptors, therefore may grow more rapidly in pregnancy
|
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what is the classic growth pattern seen in a meningioma?
|
whorling growth pattern
(also see psammoma bodies) |
|
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where do most acoustic neuromas occur?
|
involve CN VIII at the CEREBELLOPONTINE ANGLE
|
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bilateral acoustic neuromas should make you think of?
|
neurofibromatosis type II
|
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where are most cranioparyngiomas located?
|
suprasellar, in hypothalamic region
|
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germ cell neoplasms MC occur in which sex and age group?
|
young men
|
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name four germ cell neoplasms commonly seen in the CNS?
|
germinoma
choriocarcinoma embryonal carcinoma teratoma |
|
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where do CNS hemangiomas MC occur?
|
cerebellum, spinal cord
|
|
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syndrome with hereditary form of CNS hemangioma?
|
von-hippel-lindau syndrome
|
|
|
typical sites of origin of metastatic tumors to the brain?
|
melanoma
breast lung kidney |
|
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what are the 3 states of existence (according to the sleep lecturer)?
|
wakefullness
N-REM sleep REM sleep |
|
|
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 *THETA waves |
|
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describe stage II N-REM sleep
|
*K complex
*spindles *no eye mvmt |
|
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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) |
|
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in which type of sleep is HR and RR irregular?
|
REM
|
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in which type of sleep is skeletal muscle tone absent?
|
REM
|
|
|
in which type of sleep is penile tumescence and vaginal engorgement seen?
|
REM
|
|
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in which stage of sleep is poikilothermia observed?
|
REM
(that's why see sweating and chills in REM sleep) |
|
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in what type of sleep do most sleep problems occur?
|
REM sleep
|
|
|
what are the 3 mechanisms underlying wakefullness and sleep?
|
1. circadian
2. homeostatic 3. masking |
|
|
which type of sleep waves are important in cognitive maturation?
|
delta waves
|
|
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where in the brain is REM sleep initiated?
|
pons
|
|
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when are PGO waves seen?
|
REM sleep only
|
|
|
which 3 neurotransmitters have been shown to turn off REM?
|
NE
5-HT Histamine |
|
|
connection between adenosine and sleep?
|
adenosine = sleep factor
(caffeine inhibits) |
|
|
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) |
|
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what is thalamic gating?
|
shutting off of excitability coming from the lower brain centers
|
|
|
describe the effects of N-REM sleep on the following:
1. HR 2. BP 3. cerebral flow, metabolic rate |
1. decreases
2. decreases 3. decreases *remember: N-REM is primarily a PARASYMPATHETIC state* |
|
|
describe CO early in the morning
|
decreased
(that's why more MIs occur in the morning) |
|
|
what happens to the upper airway muscles in REM?
significance? |
relax
this increases airway resistance (see snoring and OSA) |
|
|
what else relaxes airway muscles?
|
etoh
benzodiazepenes |
|
|
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
|
behavioral changes during 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
snoring apneic episodes choking or gasping in sleep nocturia |
|
|
predisposing factors to OSA?
|
Age (40-60yrs)
obesity male anatomical abnormalities etoh smoking family history |
|
|
CV complications of OSA?
|
HTN
pulmonary HTN, cor pulmonale brady or tachycardia complete heart block arrythmias MI sudden death |
|
|
possible therapies for OSA?
|
1. positive airway pressure
2. oral appliances 3. surgery |
|
|
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?
|
hypocretin
|
|
|
what is the normal requirement for sleep?
|
ranges from 4-10 hrs
|
|
|
what are some medical conditions that can cause insomnia?
|
hyperthyroidism
arthritic conditions renal failure lung disease heart failure GERD hepatic disease |
|
|
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
|
|
|
define parasomnias
|
undesirable phsyical or experiential phenomena which occur exclusively during the sleep period or are exacerbated by sleep
|
|
|
3 MC parasomnias?
|
1. disorders of arousal
2. nocturnal seizures 3. REM sleep bahavior disorder |
|
|
3 disorders of arousal?
|
1. confusional arousals
2. sleepwalking 3. sleep terrors |
|
|
what are confusional arousals?
|
confusion following arousal from sleep, disorientation
|
|
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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?
|
CVA
|
|
|
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?
|
ischemic
|
|
|
three mechanisms of ischemic stroke?
|
1. large vessel
2. cardioembolic 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
2. AVM 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?
|
females
avg. age of rupture - 50 yrs |
|
|
rupture of a berry aneurysm results in what type of hemorrhage?
|
subarachnoid
|
|
|
"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
valvular disease paradoxical embolism |
|
|
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?
|
better
(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?
|
male
family Hx age HTN Afib coronary artery disease carotid artery disease DM hyperlipidemia smoking, etoh inactivity |
|
|
hematologic and cellular disoroders that predispose to stroke?
|
sickle cell
thormbocytopenia polycythemia DIC cardiolipin antibodies, lupus anticoagulants pregnancy protein C,S, antithrombin III deficiency |
|
|
s/s of an intracerebral hemorrhage?
|
*acute onset neurologic deficit
*quickly worsening *H/A, N/V *altered level of consciousness *markedly elevated BP |
|
|
s/s of subarachnoid hemorrhage?
|
*acute onet of severe H/A ("worst H/A of my life)
*meningeal signs *confusion, LOC, seizures *may progress and have focal neurologic signs |
|
|
describe the level of consciousness in an ischemic stroke
|
normal
(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
*aphasia *R hemifield loss *amaurosis fugax |
|
|
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)?
|
*incoordination/ataxia
*dysarthria *dysrhythmia *dysequilibrium *nystagmus |
|
|
symptoms of a stroke to the posterior circulation (occipital lobe)?
|
hemifield visual defect
|
|
|
symptoms of a stroke to the posterior circulation (medial temporal lobe)?
|
confusion
memory loss |
|
|
give examples of some things that mimic TIAs
|
seizures
syncope episodic vertigo migraine transient global amnesia psychosomatic |
|
|
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?
|
MRI
|
|
|
which imaging modality is better to see hemorrhage with?
|
CT
|
|
|
which imaging modality shows blood flow in vessels?
|
MRI
|
|
|
secondary prevention in a cardioembolic stroke?
|
warfarin
|
|
|
secondary prevention in a large vessel stroke?
|
carotid endarterectomy
|
|
|
secondary prevention in a small vessel stroke?
|
risk factor management
antiplatelet meds avoid anticoagulation |
|
|
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)?
|
TPA
aspirin (heparin) |
|
|
secondary prevention of ischemic strokes?
|
antiplatelet agent
control of BP, glucose and lipids coumadin carotid endarterectomy |
|
|
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
*supportive *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
|
|
|
which 2 vascular malformations require no treatment if asymptomatic?
|
venous angiomas
cavernous hemangiomas |
|
|
name 3 antiplatelet agents used in stroke prevention?
|
1. ASA
2. clopidogrel (plavix) 3. ASA/dipyridamole (aggrenox) |
|
|
Pompe's disease is primarily manifested by?
|
cardiac involvement
(cardiomegaly, CHF) |
|
|
other manifestations of Pompe's disease?
|
macroglossia/thick lips
skeletal muscle weakness failure to thrive hypotonia diminished/absent DTRs |
|
|
EMG findings in Pompe's disease?
|
pseudomyotonia
high freq. discharges fibrillations |
|
|
Pompe's disease is a deficiency in?
|
lysosomal a-1,4-glucosidase
|
|
|
chromosomal locatation of Pompe's disease mutation?
|
chromosome 17
|
|
|
inheritance pattern of Pompe's?
|
AR
|
|
|
Pathophysiology of Pompe's disease?
|
*glycogen accumulation in lysosomes of cardiac and skeletal muscle
*glycogen deposition in nervous system |
|
|
prognosis of Pompe's disease?
|
most die in 1st 2 yrs
|
|
|
which genetic myopathy is characterized by the "policeman's tip"?
|
amyoplasia congenita disruptive sequence
|
|
|
describe the facies seen in amyoplasia congenita disruptive sequence
|
round flat facies
mild micrognathia |
|
|
inheritance of amyoplasia congenita disruptive sequence?
|
none - sporadic
(could be due to intrauterine vascular accident or vascular compromise) |
|
|
pathophysiology of amyoplasia congenita disruptive sequence?
|
*hypotension in fetal spinal cord leads to decreased # of anterior horn cells
*muscle fails to form normally, get fibrous bands and fatty tissue *lack of in utero movement causes contractures |
|
|
what is the other name for cerebro-hepato-renal syndrome?
|
Zellwegger syndrome
|
|
|
facial characteristics of cerebro-hepato-renal syndrome?
|
high forehead
large fontanelles epicanthil folds flat facies |
|
|
skeletal abnormality seen in cerebro-hepato-renal syndrome?
|
patellar stippling
(Ca++ deposits visible on Xray) |
|
|
prognosis of cerebro-hepato-renal syndrome?
|
death in 1st year is common
|
|
|
inheritance pattern of cerebro-hepato-renal syndrome?
|
AR
|
|
|
pathophysiology of cerebro-hepato-renal syndrome?
|
absent to greatly reduced peroxisomes
*defect in catabolism of very long chain fatty acids *plasmalogen deficiency *phytanic acid accumulation |
|
|
which inherited disorder is characterized by furrows on the forehead when crying?
|
Miller-Dieker
(lissencephaly) |
|
|
facial characteristics of lissencephaly?
|
small anteverted nose
long philtrum thin upper lip |
|
|
where is the genetic defect in lissencephaly?
|
deletion on chromosome 17
|
|
|
pathophysiology of lissencephaly (miller-dieker)?
|
gene -> signal transduction pathway abnormality -> deficient neuronal migration -> agyria/pachygryria
|
|
|
what is the triad seen in Meckel-Gruber syndrome?
|
occipital encephalocele
polycystic kidneys postaxial polydactyly |
|
|
what is characteristic about the facial development of an individual with Meckel-Gruber?
|
absent or incomplete midfacial development
|
|
|
Meckel-Gruber involves a mutation where?
|
chromosome 17 (AR)
|
|
|
what is holoprosencephaly?
|
defect of midfacial development, incomplete forebrain development
|
|
|
possible facial characteristics of holoprosencephaly?
|
hypotelorism
absence of philtrum absence of nasal septum cyclopia proboscis cleft lip, palate |
|
|
what is the pathophysiology behind holoprosencephaly?
|
3rd-4th wk. of development: incomplete prechordial mesodermal migration to area anterior to notochord -> midfacial dysmorphogenesis and failure of forebrain division into cerebral hemispheres
|
