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- Definition: Spontaneous, uncontrolled paroxysmal,
- transitory electrical discharges, interrupts normal function. Epilepsy – condition of recurrent seizures.
- C. Pathophysiology: group of neurons function as epileptogenic
- focus. Neurons hypersensitive. Excitations spreads, causes loss of
- consciousness, muscle contraction (tonic phase)
- Inhibitory neurons react, interrupt
- seizure discharge -> causes alternating contraction and relaxation of muscles
- (clonic phase)
- Problem: oxygen use inc. lactic acid builds up -> permanent brain
D. Clincal Manifestations:
- post-ictal phase
G. Diagnostic Tests:
- EEG (electroencephalogram)
- correct or control underlying cause
a. prevent seizures – anticonvulsants
b. during seizures - valium
. Partial Seizures: begin locally
- simple partial seizure – one hemisphere, no loss of consciousness. S&S vague – fatigue, funny feeling,
- complex partial seizure – both hemispheres, change in LOC. S&S – hallucinations, sensations,
of Seizures: Generalized
- Seizures: both hemispheres, loss of consciousness.
- Absence (petit mal) – S&S:
- brief blank stare, motionless and unresponsive. 15-30 sec loss of conciousness.
- Tonic-Clonic Seizure (grand mal)
- aura S&S: first loss of consciousness. Next tonic phase – stiffening of body for
- 10-20 sec. Followed by clonic phase –
- jerking of extremeties for 30-40 sec.
- Deep resp followed by irregular shallow resp at end of seizure ->
- deep sleep.
Cerebral Vascular Accidents (CVAs)
- Definition: neurological deficits resulting from disease
- of blood vessels that supply brain.
- Blood flow interrupted: 30 secs –
- neuronal metabolism altered, 2 mins – metabolism ceases, 5 min – cell death
- B. Risk Factors: atherosclerosis, HTN, diabetes, valve
- disease, arrhythmias, coagulation disorders
- Thrombotic: brain or intracranial vessels occluded by
- thrombi that arise from arterial occlusion.
- Blood clot narrows lumen.
- Embolic: occlusion by embolus often from endocardial
- layer of heart or atherosclerotic plaques in extracranial arteries.
- Pathophysiology: Area of brain
- loses blood supply due to vascular occlusion -> ischemia -> edema,
- congestion. Thrombotic strokes develop
- slower, have prodromal signs. Embolic
- strokes develop quickly, severe manifestations.
of Strokes: Hemorrhagic
Hemorrhagic: spontaneous bleeding into brain tissue
Intracranial hemorrhage: bleeding into brain
Subarachnoid hemorrhage: bleeding into subarachnoid space
- Pathophysiology: Escaping blood
- creates mass that compresses and displaces brain -> dec in blood flow to
- brain. With large bleeds, herniation of
- brain tissue may occur. Blood also in
- ventricular system, interferes with CSF circulation -> inc ICP.
of Temporal Development:
- TIAs (transient ischemic
- attack): brief episode, no residual
- effects. Ischemic strokes.
- 2. Reversible
- ischemic neurological deficit: deficit
- remains after 24hrs but no residual S&S after few days.
- Stroke in evolution: progressing
- Complete stroke: stable when
- deficit unchanged
. Neuromotor function:
- loss of skilled voluntary mov’t (akinesia), impairment of integration of
- mov’t, alterations in muscle tone and reflex activity (hyporeflexia). Period of flaccidity (hypotonia) then
- spasticity (hypertonia).
- motor deficits: lesion on one
- side affects function on other side (contralateral)
- nutrition: difficulty feeding
- self, swallowing (dysphagia)
- 2. Communcation: dysphasia (aphasia) – dysfunction related to
- use of language and comprehension.
3. Affect: loss of control of emotions
- 4. Intellectual
- Function: memory, judgement impaired
- left sided lesions – memory problems related to language, overly
- right sided lesions – quick, impulsive
- problems with perception of self in relation to other things – neglect
- input from affected side, can be compounded by homonymous hemianopsia
- (inability so see in the same area in both eyes)
- agnosia – inability to recognize object
- apraxia – inability to carry out learned sequential mov’ts
Cerebral damage summary
- Right Cerebral Damage – left
- hemiplegia, spatial-perceptual deficits, memory deficits related to
- performance, quick and impulsive behavioral style, indifference to disabiliity
- Left Cerebral Damage – right
- hemiplegia, speech/language deficits, memory deficits related to language, slow
- and cautious behavioral style, distress and depression to disability
Tests and Treatment for Strokes
- PET – positron emission tomography
a. reduce risk factors
b. prevent further embolization
c. control cerebral edema and inc ICP
d. thrombolytic therapy
a. stop or reduce bleeding
b. control inc ICP
c. aspirate/evacuate blood
. Definition: irreversible, progressive brain disease
- B. Pathophysiology: loss of neurotransmitter stimulation with
- accumulation of amyloid proteins.
- Proteins in neurons distorted, twisted – forming neurofibrillary tangle.
- Plaques disrupt nerve impulse
C. Clinical Manifestations:
early 1. forgetfulness, short term memory loss
2. dec attention span
late 3. language skills dec
4. dec long term memory
5. faulty judgement
final 6. loss of reasoning
D. Diagnostic Tests:
- manage decline in function
- Definition: degenerative
- disorder of basal ganglia
- B. Pathophysiology: degeneration of dopamine producing neurons in
- substantia nigra of midbrain. Dec
- dopamine, inc cholinergic activity
C. Clinical Manifestations:
- dec overall activity level
E. Diagnostic Tests:
- F. Treatment: meds to control symptoms (Sinemet), physical