Exam 5: Neuro Disorders

Question 1

Stroke

Answer 1

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

Question 2

FAST

Answer 2

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

Question 3

Intracerebral hemmorhagic stroke

Answer 3

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

Question 4

Subarachnoid hemorrhagic stroke

Answer 4

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

Question 5

Patho of ischemic stroke

Answer 5

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

Question 6

Patho of hemorrhagic stroke

Answer 6

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

Question 7

Right sided vs left sided deficits

Answer 7

Question 8

TIA

Answer 8

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

Brief episode of neurological dysfunction

Warning sign of potential stroke

Question 9

TBI

Answer 9

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

Question 10

Focal and diffuse patterns of axonal injury

Answer 10

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

Question 11

Epidural hematoma

Answer 11

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

Question 12

Subdural hematoma

Answer 12

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

Question 13

Concussions

Answer 13

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

Question 14

Seizures

Answer 14

◦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

Question 15

Absence seizure

Answer 15

common in children, interrupt consciousness characterized by a blank stare

Question 16

Myoclonic seizure

Answer 16

sporadic jerks or muscle contractions

Question 17

Clonic seizures

Answer 17

sudden hypotonia

Question 18

Tonic

Answer 18

stiffening of musculature

Question 19

Atonic

Answer 19

abrupt loss of postural control, think “drop attacks”

Question 20

Epilepsy

Answer 20

chronic neurological disorder of recurrent seizures

Question 21

Status epilepticus

Answer 21

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

Question 22

Delirium

Answer 22

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

Question 23

Dementia

Answer 23

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

Question 24

Meningitis

Answer 24

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

Question 25

Monro-Kellie Hypothesis

Answer 25

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

Question 26

CM of ICP

Answer 26

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

Question 27

Multiple sclerosis

Answer 27

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

Question 28

Myasthenia gravis

Answer 28

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

Question 29

Parkinson's

Answer 29

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.

Question 30

Guillain-Barré

Answer 30

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%