Exam 5: Neuro Disorders Flashcards

1
Q

Stroke

A

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

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2
Q

FAST

A

F acial drooping
A rm weakness
S peech difficulties
T ime = brain

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3
Q

Intracerebral hemmorhagic stroke

A

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

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4
Q

Subarachnoid hemorrhagic stroke

A

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

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5
Q

Patho of ischemic stroke

A
  1. Thrombus or embolus that lodges in a cerebral artery and blocks blood flow to the brain tissue
  2. Margins of infarct blood vessels dilate
  3. Increased edema surrounding ischemia
  4. Edema leads to further perfusion problems

not always activity dependent - can happen during sleep

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6
Q

Patho of hemorrhagic stroke

A
  1. Increased ICP
  2. Ischemic cellular response
  3. Cerebral edema
  4. Compromised cerebral perfusion pressure
  5. Possible herniation-death*
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7
Q

Right sided vs left sided deficits

A
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8
Q

TIA

A

<24 hours of symptoms resolve NO INFARCT (blood flow re-established before)

Brief episode of neurological dysfunction

Warning sign of potential stroke

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9
Q

TBI

A

alteration in brain function or other evidence of brain pathology caused by an external force
sudden physical damage to the brain

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10
Q

Focal and diffuse patterns of axonal injury

A

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

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11
Q

Epidural hematoma

A

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

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12
Q

Subdural hematoma

A

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

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13
Q

Concussions

A

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

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14
Q

Seizures

A

◦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

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15
Q

Absence seizure

A

common in children, interrupt consciousness characterized by a blank stare

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16
Q

Myoclonic seizure

A

sporadic jerks or muscle contractions

17
Q

Clonic seizures

A

sudden hypotonia

18
Q

Tonic

A

stiffening of musculature

19
Q

Atonic

A

abrupt loss of postural control, think “drop attacks”

20
Q

Epilepsy

A

chronic neurological disorder of recurrent seizures

21
Q

Status epilepticus

A

continuous seizure lasting at least 5 minutes or 2 or more discrete seizures with incomplete recovery of cognition

22
Q

Delirium

A

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

23
Q

Dementia

A

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

24
Q

Meningitis

A

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

25
Q

Monro-Kellie Hypothesis

A

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

26
Q

CM of ICP

A

Change in LOC, hydrocephalus, papilledema, herniation, posturing, pupil responses, Cushing Triad (HTN w/wide pulse pressure, irregular breathing, low HR)

27
Q

Multiple sclerosis

A

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

28
Q

Myasthenia gravis

A

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

29
Q

Parkinson’s

A

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.

30
Q

Guillain-Barré

A

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%