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Neurosciences > Neurological Disorders > Flashcards

Neurological Disorders Flashcards

1
Q

CRP/ESR

A

Lab for inflammation

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2
Q

Complex regional pain syndrome

A

Pain in extremity out of proportion to initial injury
Diagnosed by having 2 or more of the following: allodynia, vasomotor changes, sudomotor changes, edema, decreased ROM, trophic changes

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3
Q

Treatment of complex regional pain syndrome

A

PT/OT
NSAIDs, AEDs, topical antioxidants, Vitamin C
Nerve blocks, epidural/ intrathecal meds
Sympathectomy
Pain management team
Palliative care team

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4
Q

Hyped of primary headaches

A

Migraine
Cluster
Tension
Other(post exercise/ coital/ cough/ etc)

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5
Q

Detailed headache assessment

A

OLDCARTS
Headaches a month
Auras
Hormonal fluctuations

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6
Q

OLD CARTS

A

Onset, location, duration, characteristics, aggravating factors, relieving factors, treatments tried, severity

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7
Q

When to worry about headaches

A

WHoL- SAH
Thunderclap- aSAH
With vigorous exercise- perimesencephalic SAH
With fever/ stiff neck - Meningitis
New onset after 50yr- tumor
With known cancer- Mets
With neuro changes
Progressive and increasing

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8
Q

Objective HA assessment

A

Neuro exam
Temporal artery tenderness
Occipital nerve tenderness
TMJ tenderness
Episodic, disabling, and w or w/o aura

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9
Q

Diagnostic tests for HA

A

ESR/ CRP to rule out temporal arteritis
Imagine to r/o structural cause
CT, MRI, CTA, MRA, MRV
LP

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10
Q

Treatment of HA

A

Mild to moderate pain
NSAIDS, muscle relaxers, heat, cold,
massage, PT
Moderate to severe pain
Triptans, ergot alkaloids
Adjunctive: anti-emetics, IV
Diphenhydramine
Education
HA diary
Prevention
Overall self care
Medications
Beta blockers, antidepressants,
AEDs, Botox

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11
Q

Status migrainosis requirement and treatment

A

Disabling migraine lasting more than 72 hours
IV migraine cocktail- VPA,
Methlyprednisolone, Mag, ketorolac,
prochlorperazine, diphenhydramine
Hydrate

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12
Q

Cluster headaches requirements and treatment

A

Rapid onset and excruciating
Medications: IV or intranasal sumatriptan, IV diphenhydramine, lidocaine nose drops, O2 7L/min for 10 minutes max

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13
Q

Definition of seizure

A

Sudden, excessive electrical discharge of neurons altering brain function and producing electrophysiological changes

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14
Q

What is epilepsy

A

Repeated unprovoked seizures

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15
Q

Focal onset seizures

A

Excessive electrical activity limited to one area
Focal Onset Aware: no chance in
awareness
Focal Onset Impaired Awareness:
Clouding of consciousness, staring,
repetitive motor behaviors
(automatisms)

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16
Q

General onset seizures

A

Excessive electrical activity that encompasses the entire brain
May start as focal
Most common forms: Tonic-clonic,
absence seizures, myoclonic

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17
Q

Unprovoked causes of epilepsy

A

Genetics
Neurodegenerative dementia
Unknown in 30-50%

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18
Q

Provoked causes of seizures

A

Acute structural injury: SAH, trauma, encephalitis, tumor, ICH, cerebral anoxia

Remote structural injury: prior trauma, CP, AVM, perinatal cerebral ischemia

Metabolic: low glucose, magnesium, sodium, calcium; high glucose, hepatic encephalopathy, uremia

Withdrawal: AEDs, benzos, ETOH, barbs, medications

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19
Q

Subjective seizure assessment

A

Detailed history: antecedent event, description of seizure, alterations in consciousness, post-ictal state, current illnesses, past medical history, social history, med list, known epilepsy history

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20
Q

Diagnostic tests for epilepsy

A

EEG
cEEG
CT/MRI
Neurophysiological testing: sodium
amobarbital, stimulation with grids

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21
Q

Interventions for seizures

A

AEDs- monotherapy if possible
Medical- ketogenic diet
Surgical interventions: VNS, Corpus
Collosotomy, lobectomy
Education
Seizure journal
Self-care

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22
Q

Psychogenic non-epileptic seizures

A

Physical manifestation of a physiologic disturbance
Diagnosed with cEEG in EMU
20-30% patient in EMU
Interventions: be transparent with dx,
education, psychotherapy

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23
Q

Status epilepticus

A

Refers to single, uninterrupted seizure greater than 5 minutes or frequent clinical seizures without a return to baseline

Types: non-convulsive or convulsive
Both types are medical emergencies

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24
Q

Risks with convulsive status epilepticus

A

Arrhythmias, aspiration, hypercapnia, lactic acidosis, and fever from the stress of continuous muscular convulsions and intense neuronal activity

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25
Q

Interventions for status epilepticus

A

ABCs!!!!
Neuro assessment to classify type
Supportive ventilation
Initial meds: lorazepam 0.1mg/kg
Phenytoin: 20mg/kg @50mg/min
Fosphenytoin: 20mg PE/kg @100-120
pe/ min
If hypoglycemia is suspected: 100mg thiamine then 50cc of D50
Continue ABCs: intubate if needed
Treat metabolic abnormalities
Continuous EEG
Refractory infusions: midazolam,
propofol, pentobarbital
Super-refractory: ketogenic diet,
ketamine, ECT

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26
Q

Hydrocephalus

A

Results from an imbalance between CSF inflow and outflow

Caused by obstruction, inadequate absorption, or over production

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27
Q

Types of hydrocephalus

A

Congenital

Acquired: non-communicating, communicating, normal pressure

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28
Q

CSF fluid pathway

A

Lateral ventricles, foramen of monro, third ventricle, cerebral aqueduct of sylvius, fourth ventricle, foramen of luschka and magendie, subarachnoid space, arachnoid villi, venous drainage system

29
Q

Assessment finding in hydrocephalus

A

Headache
Nausea and vomiting
Drowsiness
Decreased LOC
upward gaze palsy
Late sign: pupillary changes

30
Q

Interventions for hydrocephalus

A

EVD
Shunt
Endoscopic third ventriculostomy
Acetazolamide

31
Q

Idiopathic intracranial hypertension

A

Also called pseudotumor cerebri
Signs and symptoms: headache, papilledema, visual abnormalities
Subjective findings: pulsation tinnitus, back pain, retrobulbar pain, diplopia, sustained visual loss, neck pain, transient visual obscurations
Objective findings: visual field loss, papilledema, sixth nerve palsy

32
Q

Diagnostic tests for idiopathic intracranial hypertension

A

Ophthalmologic exam
CT/MRI
LP to get opening pressure
CTV

33
Q

Interventions for idiopathic intracranial hypertension

A

Observation- if vision intact and
minimal symptoms
Medical- weight loss, carbonic
anhydrase inhibitors, acetazolamide
topiramate, headache management
Surgical- optic nerve fenestration,
shunt, venous sinus
stenting(controversial)

34
Q

Acute Encephalopathy

A

A rapidly developing pathobiological process in the brain

Develops in less than 4 weeks but usually a few hours to days

35
Q

Types of encephalopathy

A

Toxic metabolic

Posterior reversible encephalopathy syndrome

36
Q

Toxic metabolic encephalopathy

A

Acute global cerebral dysfunction in the absence of primary structural brain disease
Encompasses delirium
Consequence of systemic disease

37
Q

Causes of toxic metabolic encephalopathy

A

Drugs
Electrolyte imbalance
Lack of drugs (withdrawal/ uncontrolled pain)
Infection
Reduced sensory input
Intracranial (stroke, SDH)
Urinary retention or fecal impaction
Myocardial or pulmonary

38
Q

Interventions for toxic metabolic encephalopathy

A

Thiamine
Sensory enhancement
Avoid restraints
Treat underlying cause
Antipsychotics for agitation such as seroquel or haloperidol

39
Q

Prevention of toxic metabolic encephalopathy

A

Eliminate unnecessary meds
D/C catheter
Regulation of bowel and bladder function
Adequate nutritional intake
Early mobilization and rehab

40
Q

Posterior reversible encephalopathy syndrome

A

Clinical syndrome of headache, confusion, decreased LOC, visual changes, and seizures

Associated with neuro imaging findings of posterior cerebral white matter edema

41
Q

Other names for PRES

A

Reversible posterior leukoencephalopathy syndrome

Reversible posterior cerebral edema syndrome

Hyperperfusion syndrome

Brain capillary leak syndrome

42
Q

Causes of PRES

A

Hypertensive encephalopathy
Acute or chronic kidney disease
Immunosuppressive,
immunomodulatory, and
chemotherapeutic drugs
Hemolytic and uremic syndrome
Eclampsia
Vasculitis
Hypercalcemia
Hypomagnesemia
Iodine contrast exposure
Sepsis
Post transplant

43
Q

Symptoms of toxic metabolic encephalopathy

A

Mental status ranged from subtle changes to delirium or coma

Delirium- acute onset confusion, agitation, psychomotor slowing

Motor- tremor, asterixis bilaterally, myoclonus, primitive reflexes, brisk DTRs

44
Q

Subjective assessment finding with PRES

A

Headache
Vision loss
Hallucinations
Auras

45
Q

Objective findings in PRES

A

Somnolence
Confusion
Agitation
Coma
Hemianopia
Seizures

46
Q

Interventions for PRES

A

BP management with gradual decrease within 2-6 hours and no more than 25% less than presenting BP. Usually with easily titratable agents

Treat seizures

D/C immunotherapy

Pregnancy- called Eclampsia over PRES. Deliver baby and placenta. Seizure meds and anti hypertensives may be different

47
Q

Complications of PRES

A

Stroke

Ischemic
Hemorrhagic (ICH or convexal SAH) more common in patients with underlying coagulopathy

48
Q

Prognosis of PRES

A

Usually benign. Remove inciting factor and control BP. Fully reversible within period of days to weeks

Death may occur if progressive cerebral edema, large ICH, or from an underlying condition

49
Q

Dementia

A

Intellectual deterioration that interferes with social or occupational performance.

Features impairment in:
Long and short term memory
Abstract thinking
Judgement
Cortical functions

50
Q

Classifications of dementia

A

Alzheimer’s
Vascular
Lewy body
Frontal lobe deterioration
Mixed
Parkinson’s
CJD
Multifocal leukoencephalopathy

51
Q

Diagnostic tests for dementia

A

Biomarkers in CSF (beta-amyloid)
MRI/PET looking for neuro degenerative changed
Rule out other reversible causes

Cognitive testing such as MMSE and Mini-cog

52
Q

Medications for dementia

A

Cholinesterase inhibitors like Aricept

NMDA agonists- Namenda

53
Q

Parkinson’s Disease

A

Neurodegenerative disorder caused by the depletion of dopamine producing cells in the substantia nigra

54
Q

Classical Parkinson’s presentation

A

Asymmetrical
Resting tremor
Rigidity
Bradykinesia
Diminished postural stability

55
Q

Subjective Parkinson’s findings

A

Unilateral tremor
Difficulty with fine motor skills
Difficulty with ADLs
Gait abnormalities

56
Q

Objective Parkinson’s findings

A

Motor triad
- resting tremor
- bradykinesia
- rigidity
Postural instability
Stooped shuffling gait
Autonomic dysfunction
Parasthesias
Craniofacial abnormalities

57
Q

Medications for Parkinson’s

A

Sinemet (carbidopa/levidopa)
Dopamine agonistsa (requip, mirapex)
Anticholinergics (artane, cogentin)

58
Q

Surgical options for Parkinson’s

A

Deep brain stimulator
Ablation- pallidotomy, thalamotomy

59
Q

Parkinsonism

A

Differentiated from Parkinson’s by absence of bradykinesia and rigidity

Essential tremors usually bilateral

60
Q

Medications for Parkinsonism

A

Propranolol
Primidone
Gabapentin
Topiramate

61
Q

Dystonia

A

Movement disorder
Involuntary, sustained, or intermittent muscle contractions
Force limbs into painful, twisting, repetitive movements or postures

62
Q

Clinical findings in dystonia

A

Blepharospasm
Writers cramp
Laryngeal dystonia
Cervical torticollis

63
Q

Interventions for dystonia

A

Exercise
PT
Psychosocial support
Medications
Deep brain stimulation

64
Q

Causes of peripheral nerve injury

A

Trauma
Nerve entrapment
-median (carpal tunnel)
-ulnar
-radial
-brachial plexus (neurogenic thoracic outlet syndrome
-peroneal
-lateral femoral

65
Q

Assessment findings with peripheral nerve injury

A

Subjective
- pain
- paresthesia

Objective
- weakness
- sensory loss

66
Q

Treatment for peripheral nerve injury

A

Open traumatic- always surgical

Closed traumatic and entrapment- surgical if no improvement after conservative measures such as PT/OT and splinting in 3 months

67
Q

Minor alcohol withdrawal symptoms

A

Insomnia, mild anxiety, GI upset, anorexia, headache, diaphoresis, palpitations, tremors

Set in 6-36 hours after the last drink

68
Q

Moderate and severe alcohol withdrawal symptoms

A

Seizure (6-48hrs after)

Hallucination (12-48hrs after)

DT’s: delirium, agitation, tachycardia, hypertension, fever, and diaphoresis (48-96hrs after)

69
Q

Opiate withdrawal

A

4 - 48 hours after last use

Naturally occurring withdrawal is not life threatening

Iatrogenic withdrawal must be administered slowly as it is potentially life threatening

Symptoms: mydriasis, yawning, diaphoresis, piloerection, dysphoria, restlessness, rhinorrhea, lacrimation, myalgias, arthralgias, nausea, vomiting, abdominal cramping, diarrhea, tachycardia, hypertension

Neurosciences (5 decks)

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