Stroke Flashcards
CNS vs PNS
CNS -UMN: cortical, brainstem, spinal cord -other: basal ganglia, cerebellum, other PNS -LMN: CN motor nuclei -other: CN sensory and special
neuroanatomy: MCA
face mainly contralateral hemiparesis sensory loss homonymous hemianopsia dominant hemisphere (L MCA): Aphsia non-dominant (R MCA): impaired spatial perception and contralateral neglect
neuroanatomy: ACA
supplies primarily medial frontal and parietal lobes
deficits: contralateral LE weakness, and sensory loss
neuroanatomy: PCA
supplies
-small penetrating arteries to midbrain and thalalmus
-occipital lobes and inferior medial temporal lobe
deficits
-homonymous hemianopsia, alexia, sensory loss
neuroanatomy: brainstem
medulla: vertebral and PICA
pons: basilar, ACIA, SCA
midbrain: PCA
general deficits
-LOC, nausea, vomiting, hemiparesis, CN involvement, can have crossed signs (ipsilateral face, contralateral body), can have ipsilateral cerebellar signs
neuroanatomy: lacunar syndromes
small location-big consequences (internal capsule)
occlusions of single small perforating arteries
definition
rapidly developing clinical signs of focal (at times global) disturbance of cerebral function, lasting for more than 24 hours or leading to death, with no apparent cause other than of vascular origin
prevalence/incidence
prevalence: older adults, blacks, lower levels of education, living in the southeastern US
incidence: every 40 sec someone in the US has a stroke
mortality/morbidity
every 4 min., someone dies of a stroke
the leading cause of serious long-term disability in the US
hemorrhagic stroke has higher mortality than ischemic
etiology
ischemic: 70-80%
hemorrhagic: 20%
- intraparenchymal or intracerebral hemorragic: 10-15%
- subarachnoid hemorrhage: 5%
pathogenesis: ischemic
partial or complete loss of blood suply to an area of the brain
causes: embolic, thrombotic/atherosclerotic, lacunar, cryptogenic, arterial dissection
disease course
focal neurologic deficits in minutes
seen by MD in 10-15 min
CT scan and interpret 25-45 min
if ischemic need treatment by rTPA within 3 hours
stable in hospital and then IP rehab or SNF
most rapid recovery in first 3-6 months
chronic lifetime recovery
ischemic: s/s
sudden onset of focal neurological deficits
symptoms in minutes
headache
nausea and vomiting (brainstem and cerebellum)
acute HTN
act FAST
ischemic: risk factors
hypertension cardiac disease diabetes hyperlipidemia smoking carotid artery stenosis TIA
diagnosis
from history, neuro exam, and imaging
CT, MRI, carotid US, echo, ECG
ischemic CVA prognosis
30 day mortality rate reoccurrance -3-10% in first 30 days -2-20% per year 3-6 months post (85%) walk independently
hemorrhagic CVA general considerations
IPH or ICH: bleeding within the brain
SAH: vessel rupture in subarachnoid space
hemorrhagic CVA pathogensis
hematoma forms, edema (peaks at 48 hrs, resolves by 5 days), tissue shifts
hemorrhagic CVA causes
HTN cerebral amyloid angiopathy vascular malformations drug use neoplasm anticoagulaiton therapy
common IPH sites
lobar basal ganglia/internal capsule thalamic pontine cerebellar
IPH s/s
focal deficit that worsens over minutes
acute HTN
headache
large hematomas: nausea, vomiting, early decline in level of consciousness
IPH risk factors
HTN
IPH diagnostic tests
CT scan
MRI
lab tests
SAH general considertions
bleeding into subarachnoid space 5-10 5 of all CVAs mortality is high: 25-50% causes: ruptured aneurysm, vascular malformation
SAH clinical findings
sudden onset severe headache
neurologic signs
LOC, coma
SAH diagnostic tests
CT scan
catheter angiographyy
MRI (cranial and possibly cervical and thoracic)
lumbar puncture
stroke: acute medical management
ischemic: rTPA (given within 3-4.5 hrs of stroke)
ischemic: antiplatelet (apsirin) within 48 hrs
blood pressure measurement
surgery
stroke: complications
hemorrhagic transformation for infarcts
brain edema
seizures
medical complications (aspiration pneumonia, UTI, DVT, hyperglycemia)
better prognostic factors
ischemic
hemorrhagic for recovering function
younger age
worse prognostic factors
age (>75) high blood glucose history of prior CVA more severe CVA urinary incontinence
implications for PT management
recovery
-flaccidity initially, then spasticity
-spontaneous recovery in first 3-6 months, but continued recovery possible in chronic stages
neuroplasticity
