Exam 5: Neuro Disorders Flashcards
Stroke
Etiology: Endothelial injury, Arteriosclerosis, Hypertension, Hyperlipidemia, Diabetes, Atrial Fibrillation, Overweight/obesity, Previous TIA, Sickle cell, Tobacco use, Alcohol use, Physical inactivity, Oral contraceptives, Family history, Age/gender
CM: Think FAST; sudden AMS or HA
Diagnostics: History and presentation, LOC, GCS, CT/MRI, NIHSS, Opthalmoscopic exam
FAST
F acial drooping
A rm weakness
S peech difficulties
T ime = brain
Intracerebral hemmorhagic stroke
Intracerebral (*most common type of hemorrhagic stroke)
Etiology: HTN, trauma, arteriovenous malformation (AVM)
Ruptured of cerebral blood flow bleeding into the brain -> adjacent brain is contused, swollen, and incomplete return of function
Subarachnoid hemorrhagic stroke
Etiology: HTN, trauma, aneurysm, cigarette smoking, use of high estrogen oral contraceptives, excessive alcohol intake, use of illegal drugs
Ruptured vessel in subarachnoid space
Interferes with cerebral spinal fluid (CSF) reabsorption, hydrocephalus results.
Leads to vasospasms
Patho of ischemic stroke
- Thrombus or embolus that lodges in a cerebral artery and blocks blood flow to the brain tissue
- Margins of infarct blood vessels dilate
- Increased edema surrounding ischemia
- Edema leads to further perfusion problems
not always activity dependent - can happen during sleep
Patho of hemorrhagic stroke
- Increased ICP
- Ischemic cellular response
- Cerebral edema
- Compromised cerebral perfusion pressure
- Possible herniation-death*
Right sided vs left sided deficits
TIA
<24 hours of symptoms resolve NO INFARCT (blood flow re-established before)
Brief episode of neurological dysfunction
Warning sign of potential stroke
TBI
alteration in brain function or other evidence of brain pathology caused by an external force
sudden physical damage to the brain
Focal and diffuse patterns of axonal injury
DAI occurs when the brain moves back and forth in the skull, hitting into the cranial bone, as a result of coup-contrecoup injury -> mild to severe depending on length of coma and deficits
Epidural hematoma
Serious head injury w/hx trauma: caused due to skull bone fracture
Bleeding epidural space
Arterial based: FAST (“worse HA of life”)
transient loss of consciousness →”lucid interval“→ rapid decline
Delayed in recognition causes death
Subdural hematoma
Most common type of traumatic intracranial hematoma w/hx of trauma
Bleeding below the dura matter and above the arachnoid membrane
The subdural hematoma occurs from tearing of bridging veins located in the subdural space.
Venous based: slow
Acute within 72 hours, subacute can take up to 7 days to accumulate
Occur in the elderly, anticoagulants, alcoholics
Concussions
Trauma-induced AMS that may or may not involve LOC (mild TBI)
Patho: Physiological disruption in brain function caused by traumatic forces
Simple: Resolve few hours to 10 days
Complex: prolong loss of consciousness, prolonged impairment months to years, seizures
Altered LOC, HA, Dizzy, lack of coordination , Imbalance, Amnesia, Vomiting may suggest elevated ICP
Seizures
◦single event of abnormal discharge that results in an abrupt and temporary altered state of cerebral function
focal/partial or generalized
Patho: Imbalance between excitation and inhibition of CNS
Need excitable neurons
Increase in excitatory glutaminergic activity for recurrent connection to spread discharge
Reduction in activity of the normal inhibitory (GABA) projection
Risk factors/causes: head trauma (young), stroke (elderly), genetics
Diagnosed: history and physical and EEG
Absence seizure
common in children, interrupt consciousness characterized by a blank stare
Myoclonic seizure
sporadic jerks or muscle contractions
Clonic seizures
sudden hypotonia
Tonic
stiffening of musculature
Atonic
abrupt loss of postural control, think “drop attacks”
Epilepsy
chronic neurological disorder of recurrent seizures
Status epilepticus
continuous seizure lasting at least 5 minutes or 2 or more discrete seizures with incomplete recovery of cognition
Delirium
Rapid onset
Primary -> defect in attention
Fluctuates during the course of a day
Visual hallucinations common
Often CANNOT attend to Mini-Mental Status Exam (MMSE) or clock draw
Dementia
Insidious onset
Primary -> defect in short term memory
Attention often normal
Does not fluctuate during day
Visual hallucinations less common
CAN attend to MMSE or clock draw, but cannot perform well
Meningitis
Etiology: bacterial or viral, close contact
Patho: inflammation of the pia mater, the arachnoid, and the CSF fill subarachnoid space
CM: Nuchal rigidity or the neck stiffness
Diagnosis: lumbar puncture, purulent CSF
Prognosis: depends on treatment
Monro-Kellie Hypothesis
The body can adjust to changes in pressure in several ways:
1. Displacement of CSF from ventricles
2. Displacement of blood by low pressure venous system
3. Decreased production of CSF
4. Vasoconstriciton of cerebral vasculature
CM of ICP
Change in LOC, hydrocephalus, papilledema, herniation, posturing, pupil responses, Cushing Triad (HTN w/wide pulse pressure, irregular breathing, low HR)
Multiple sclerosis
autoimmune inflammatory disorder - r/t genetics, viral or infectious process
affects women more than men, 20-late 40s
T-cells attack the myelin of the CNS -> damage to the myelin slows or prevents neurological signals from passing through so movement is impaired
myelin repairs but plaques are formed
relapsing-remitting form of MS is the most common where there are brief episodes of damage followed full or incomplete recovery
CM: weakness, numbness, tingling, sensations, balance problems, blurred vision, fatigue, optic neuritis, bowel/bladder dysfunction or Lhermitte’s sign (electric shock radiating down the spine or into the limbs most often after flexion of the neck)
Early signs
involve visual changes for many patients & cerebellar damage -> ataxia, tremor, and dysarthria
Late signs
severe motor nerve damage, dysphagia
MRI & hx - prognosis: chronic and attempt to lesson exacerbations
Myasthenia gravis
Autoimmune disease caused by the loss of functioning acetylcholine (Ach) receptors in the neuromuscular junction -> Antibodies attack the Acetylcholine (Ach) receptors
inefficient neuromuscular transmission, which is manifested as muscle weakness and easy fatigability
Early and predominant findings -> ptosis and diplopia
Difficulty with speech and neck muscles involvement
85% develop generalized weakness
Diagnosis: Most individuals with MG test positive for Ach receptor antibodies, if AChR is negative may be positive for MuSK autoantibodies, nerve conduction studies
Prognosis: can be in sustained remission (treatable) and prevent exacerbations or fatal
Parkinson’s
Etiology: Unknown. Genetics, age, and/or environment factors are associated with the disease; accumulation of an abnormal protein but it is unclear how it causes this disorder
Dopamine depletion due to the loss of dopamine-producing neuron cells in the substantia nigra -> creates an imbalance between acetylcholine (stimulates muscle movement) and dopamine neurotransmitters
Classic three symptoms -> bradykinesia, resting tremor or pin rolling, muscle rigidity (cogwheel or ratchet movement)
Could have facial stare or blank stare, shuffling gait, low monotone, depression, dementia, sleep disturbances.
Diagnosed around 50-60 by hx, No specific definitive test -> Could get a PET scan looking for Lewy bodies
Prognosis: Slow insidious onset with continued deterioration and progressive difficulty with automatic movement, no cure.
Guillain-Barré
Etiology: autoimmune disorder seen after an upper respiratory tract infection or gastroenteritis. (Cytomegalovirus (CMV), Epstein-Barr, mycoplasma pneumonia, C. Jejuni)
Epi: more frequently in men than women, more often in the elderly population
A previous infection evokes an autoimmune response that causes demyelination of the cranial and spinal nerves → edema and inflammation of peripheral nerves (flaccid paralysis & progressive limb weakness)
3 stages : Acute - 1-3 weeks; Plateau - few days - 2 weeks; Recovery - up to two years
Progressive symmetric muscle weakness, accompanied by absent or depressed deep tendon reflexes. ascending paralysis, sensory and motor nerve involvement
Diagnosis: History of recent infection, EMG, past medical history
Prognosis: there is no cure and can be fatal without interventions depending on the amount of paralysis
Full recovery for about 60%
