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Neurological Disorders Flashcards

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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
Interventions for status epilepticus
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
26
Hydrocephalus
Results from an imbalance between CSF inflow and outflow Caused by obstruction, inadequate absorption, or over production
27
Types of hydrocephalus
Congenital Acquired: non-communicating, communicating, normal pressure
28
CSF fluid pathway
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
Assessment finding in hydrocephalus
Headache Nausea and vomiting Drowsiness Decreased LOC upward gaze palsy Late sign: pupillary changes
30
Interventions for hydrocephalus
EVD Shunt Endoscopic third ventriculostomy Acetazolamide
31
Idiopathic intracranial hypertension
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
Diagnostic tests for idiopathic intracranial hypertension
Ophthalmologic exam CT/MRI LP to get opening pressure CTV
33
Interventions for idiopathic intracranial hypertension
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
Acute Encephalopathy
A rapidly developing pathobiological process in the brain Develops in less than 4 weeks but usually a few hours to days
35
Types of encephalopathy
Toxic metabolic Posterior reversible encephalopathy syndrome
36
Toxic metabolic encephalopathy
Acute global cerebral dysfunction in the absence of primary structural brain disease Encompasses delirium Consequence of systemic disease
37
Causes of toxic metabolic encephalopathy
**D**rugs **E**lectrolyte imbalance **L**ack of drugs (withdrawal/ uncontrolled pain) **I**nfection **R**educed sensory input **I**ntracranial (stroke, SDH) **U**rinary retention or fecal impaction **M**yocardial or pulmonary
38
Interventions for toxic metabolic encephalopathy
Thiamine Sensory enhancement Avoid restraints Treat underlying cause Antipsychotics for agitation such as seroquel or haloperidol
39
Prevention of toxic metabolic encephalopathy
Eliminate unnecessary meds D/C catheter Regulation of bowel and bladder function Adequate nutritional intake Early mobilization and rehab
40
Posterior reversible encephalopathy syndrome
Clinical syndrome of headache, confusion, decreased LOC, visual changes, and seizures Associated with neuro imaging findings of posterior cerebral white matter edema
41
Other names for PRES
Reversible posterior leukoencephalopathy syndrome Reversible posterior cerebral edema syndrome Hyperperfusion syndrome Brain capillary leak syndrome
42
Causes of PRES
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
Symptoms of toxic metabolic encephalopathy
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
Subjective assessment finding with PRES
Headache Vision loss Hallucinations Auras
45
Objective findings in PRES
Somnolence Confusion Agitation Coma Hemianopia Seizures
46
Interventions for PRES
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
Complications of PRES
Stroke Ischemic Hemorrhagic (ICH or convexal SAH) more common in patients with underlying coagulopathy
48
Prognosis of PRES
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
Dementia
Intellectual deterioration that interferes with social or occupational performance. Features impairment in: Long and short term memory Abstract thinking Judgement Cortical functions
50
Classifications of dementia
Alzheimer’s Vascular Lewy body Frontal lobe deterioration Mixed Parkinson’s CJD Multifocal leukoencephalopathy
51
Diagnostic tests for dementia
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
Medications for dementia
Cholinesterase inhibitors like Aricept NMDA agonists- Namenda
53
Parkinson’s Disease
Neurodegenerative disorder caused by the depletion of dopamine producing cells in the substantia nigra
54
Classical Parkinson’s presentation
Asymmetrical Resting tremor Rigidity Bradykinesia Diminished postural stability
55
Subjective Parkinson’s findings
Unilateral tremor Difficulty with fine motor skills Difficulty with ADLs Gait abnormalities
56
Objective Parkinson’s findings
Motor triad - resting tremor - bradykinesia - rigidity Postural instability Stooped shuffling gait Autonomic dysfunction Parasthesias Craniofacial abnormalities
57
Medications for Parkinson’s
Sinemet (carbidopa/levidopa) Dopamine agonistsa (requip, mirapex) Anticholinergics (artane, cogentin)
58
Surgical options for Parkinson’s
Deep brain stimulator Ablation- pallidotomy, thalamotomy
59
Parkinsonism
Differentiated from Parkinson’s by absence of bradykinesia and rigidity Essential tremors usually bilateral
60
Medications for Parkinsonism
Propranolol Primidone Gabapentin Topiramate
61
Dystonia
Movement disorder Involuntary, sustained, or intermittent muscle contractions Force limbs into painful, twisting, repetitive movements or postures
62
Clinical findings in dystonia
Blepharospasm Writers cramp Laryngeal dystonia Cervical torticollis
63
Interventions for dystonia
Exercise PT Psychosocial support Medications Deep brain stimulation
64
Causes of peripheral nerve injury
Trauma Nerve entrapment -median (carpal tunnel) -ulnar -radial -brachial plexus (neurogenic thoracic outlet syndrome -peroneal -lateral femoral
65
Assessment findings with peripheral nerve injury
Subjective - pain - paresthesia Objective - weakness - sensory loss
66
Treatment for peripheral nerve injury
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
Minor alcohol withdrawal symptoms
Insomnia, mild anxiety, GI upset, anorexia, headache, diaphoresis, palpitations, tremors Set in 6-36 hours after the last drink
68
Moderate and severe alcohol withdrawal symptoms
Seizure (6-48hrs after) Hallucination (12-48hrs after) DT’s: delirium, agitation, tachycardia, hypertension, fever, and diaphoresis (48-96hrs after)
69
Opiate withdrawal
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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