Neurological Disorders Flashcards
CRP/ESR
Lab for inflammation
Complex regional pain syndrome
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
Treatment of complex regional pain syndrome
PT/OT
NSAIDs, AEDs, topical antioxidants, Vitamin C
Nerve blocks, epidural/ intrathecal meds
Sympathectomy
Pain management team
Palliative care team
Hyped of primary headaches
Migraine
Cluster
Tension
Other(post exercise/ coital/ cough/ etc)
Detailed headache assessment
OLDCARTS
Headaches a month
Auras
Hormonal fluctuations
OLD CARTS
Onset, location, duration, characteristics, aggravating factors, relieving factors, treatments tried, severity
When to worry about headaches
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
Objective HA assessment
Neuro exam
Temporal artery tenderness
Occipital nerve tenderness
TMJ tenderness
Episodic, disabling, and w or w/o aura
Diagnostic tests for HA
ESR/ CRP to rule out temporal arteritis
Imagine to r/o structural cause
CT, MRI, CTA, MRA, MRV
LP
Treatment of HA
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
Status migrainosis requirement and treatment
Disabling migraine lasting more than 72 hours
IV migraine cocktail- VPA,
Methlyprednisolone, Mag, ketorolac,
prochlorperazine, diphenhydramine
Hydrate
Cluster headaches requirements and treatment
Rapid onset and excruciating
Medications: IV or intranasal sumatriptan, IV diphenhydramine, lidocaine nose drops, O2 7L/min for 10 minutes max
Definition of seizure
Sudden, excessive electrical discharge of neurons altering brain function and producing electrophysiological changes
What is epilepsy
Repeated unprovoked seizures
Focal onset seizures
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)
General onset seizures
Excessive electrical activity that encompasses the entire brain
May start as focal
Most common forms: Tonic-clonic,
absence seizures, myoclonic
Unprovoked causes of epilepsy
Genetics
Neurodegenerative dementia
Unknown in 30-50%
Provoked causes of seizures
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
Subjective seizure assessment
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
Diagnostic tests for epilepsy
EEG
cEEG
CT/MRI
Neurophysiological testing: sodium
amobarbital, stimulation with grids
Interventions for seizures
AEDs- monotherapy if possible
Medical- ketogenic diet
Surgical interventions: VNS, Corpus
Collosotomy, lobectomy
Education
Seizure journal
Self-care
Psychogenic non-epileptic seizures
Physical manifestation of a physiologic disturbance
Diagnosed with cEEG in EMU
20-30% patient in EMU
Interventions: be transparent with dx,
education, psychotherapy
Status epilepticus
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
Risks with convulsive status epilepticus
Arrhythmias, aspiration, hypercapnia, lactic acidosis, and fever from the stress of continuous muscular convulsions and intense neuronal activity
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
Hydrocephalus
Results from an imbalance between CSF inflow and outflow
Caused by obstruction, inadequate absorption, or over production
Types of hydrocephalus
Congenital
Acquired: non-communicating, communicating, normal pressure
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
Assessment finding in hydrocephalus
Headache
Nausea and vomiting
Drowsiness
Decreased LOC
upward gaze palsy
Late sign: pupillary changes
Interventions for hydrocephalus
EVD
Shunt
Endoscopic third ventriculostomy
Acetazolamide
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
Diagnostic tests for idiopathic intracranial hypertension
Ophthalmologic exam
CT/MRI
LP to get opening pressure
CTV
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)
Acute Encephalopathy
A rapidly developing pathobiological process in the brain
Develops in less than 4 weeks but usually a few hours to days
Types of encephalopathy
Toxic metabolic
Posterior reversible encephalopathy syndrome
Toxic metabolic encephalopathy
Acute global cerebral dysfunction in the absence of primary structural brain disease
Encompasses delirium
Consequence of systemic disease
Causes of toxic metabolic encephalopathy
Drugs
Electrolyte imbalance
Lack of drugs (withdrawal/ uncontrolled pain)
Infection
Reduced sensory input
Intracranial (stroke, SDH)
Urinary retention or fecal impaction
Myocardial or pulmonary
Interventions for toxic metabolic encephalopathy
Thiamine
Sensory enhancement
Avoid restraints
Treat underlying cause
Antipsychotics for agitation such as seroquel or haloperidol
Prevention of toxic metabolic encephalopathy
Eliminate unnecessary meds
D/C catheter
Regulation of bowel and bladder function
Adequate nutritional intake
Early mobilization and rehab
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
Other names for PRES
Reversible posterior leukoencephalopathy syndrome
Reversible posterior cerebral edema syndrome
Hyperperfusion syndrome
Brain capillary leak syndrome
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
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
Subjective assessment finding with PRES
Headache
Vision loss
Hallucinations
Auras
Objective findings in PRES
Somnolence
Confusion
Agitation
Coma
Hemianopia
Seizures
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
Complications of PRES
Stroke
Ischemic
Hemorrhagic (ICH or convexal SAH) more common in patients with underlying coagulopathy
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
Dementia
Intellectual deterioration that interferes with social or occupational performance.
Features impairment in:
Long and short term memory
Abstract thinking
Judgement
Cortical functions
Classifications of dementia
Alzheimer’s
Vascular
Lewy body
Frontal lobe deterioration
Mixed
Parkinson’s
CJD
Multifocal leukoencephalopathy
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
Medications for dementia
Cholinesterase inhibitors like Aricept
NMDA agonists- Namenda
Parkinson’s Disease
Neurodegenerative disorder caused by the depletion of dopamine producing cells in the substantia nigra
Classical Parkinson’s presentation
Asymmetrical
Resting tremor
Rigidity
Bradykinesia
Diminished postural stability
Subjective Parkinson’s findings
Unilateral tremor
Difficulty with fine motor skills
Difficulty with ADLs
Gait abnormalities
Objective Parkinson’s findings
Motor triad
- resting tremor
- bradykinesia
- rigidity
Postural instability
Stooped shuffling gait
Autonomic dysfunction
Parasthesias
Craniofacial abnormalities
Medications for Parkinson’s
Sinemet (carbidopa/levidopa)
Dopamine agonistsa (requip, mirapex)
Anticholinergics (artane, cogentin)
Surgical options for Parkinson’s
Deep brain stimulator
Ablation- pallidotomy, thalamotomy
Parkinsonism
Differentiated from Parkinson’s by absence of bradykinesia and rigidity
Essential tremors usually bilateral
Medications for Parkinsonism
Propranolol
Primidone
Gabapentin
Topiramate
Dystonia
Movement disorder
Involuntary, sustained, or intermittent muscle contractions
Force limbs into painful, twisting, repetitive movements or postures
Clinical findings in dystonia
Blepharospasm
Writers cramp
Laryngeal dystonia
Cervical torticollis
Interventions for dystonia
Exercise
PT
Psychosocial support
Medications
Deep brain stimulation
Causes of peripheral nerve injury
Trauma
Nerve entrapment
-median (carpal tunnel)
-ulnar
-radial
-brachial plexus (neurogenic thoracic outlet syndrome
-peroneal
-lateral femoral
Assessment findings with peripheral nerve injury
Subjective
- pain
- paresthesia
Objective
- weakness
- sensory loss
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
Minor alcohol withdrawal symptoms
Insomnia, mild anxiety, GI upset, anorexia, headache, diaphoresis, palpitations, tremors
Set in 6-36 hours after the last drink
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)
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
