Exam 7 Flashcards
Migraines effect up to…
12% of the population, more women
Migraine pathophysiology
Genetically predisposed hyperexcitable neurovascular system
Cortical spreading, vasodilation and inflammation
Migraine prodrome
60% of migraine sufferers
24-48 hours before HA
Euphoria/ depression/ irritability Food cravings Constipation Neck stiffness Increased yawning
Migraine aura
25% of migraine sufferers
Visual (most common)
Sensory
Verbal
Motor
Less than one hour!! Completely reversible
Visual aura of migraine
Field defects Luminous visual hallucinations Scintillating scotomas (field defects and luminous visual hallucinations)
Motor aura
Familial hemiplegic migraine- autosomal dominant, fully reversible motor weakness
Sporadic hemiplegic migraine- no relative has had an attack
Migraine HA characteristics
4-72 hours
At least 2: Unilateral Pulsating or throbbing Moderate or severe Aggravated by physical activity
NV, photophobia or photophobia
Migraine postdrome
Sudden head movement causes pain, exhaustion, mild elation or euphoria
Migrainous vertigo
Recurrent episodic vertigo in a patient with migraines
Basilar type migraine
Migraine with aura symptoms that come from the brainstem and/or both hemispheres simultaneously
NO MOTOR WEAKNESS
At least two of these fully reversible stroke like symptoms
Retinal/ocular migraine
Repeated attacks of monocular scotoma or blindness, less than 1 hour
Followed by HA
Irreversible visual loss is common here
Ophthalmoplegic migraine
Lateralized eye pain with NV, diplopia
HA for a week or more, latent period of around 4 days before ophthalmoplegia
Consider prophylaxis for migraines if…
2 or three migraines per month or significant disability with attacks
Tension headache epidemiology
86% prevalence, more women than men
TTH patho
Heightened sensitivity of pain pathways
Increased muscle tenderness
TTH presentation
Vise like, tight
Neck or back of head
Generalized and bilateral
Mild to moderate
No neuro symptoms!
Three main types of TTH
Infrequent episodic- less than 1 day a month
Frequent episodic- 1-14 days per month
Chronic- greater than 15 days per month
Duration and at least 2 of these for TTH
30 min -7 days for episodic
Pressing/tightening
Mild to moderate
Bilateral
Not aggrated by routine physical activity
*no NV, no photobia or phonophobia
Cluster headache presentation
Severe pain Orbital, temporal, supraorbital Strictly unilateral At night, awake the patient Autonomic phenomena Restless, pacing, rocking back and forth
Cluster headache timing
Up to 8 times a day
Short lived, 15 minutes to 3 hours
Cluster period can last 6-12 weeks
Remissions can last 12 months even
Autonomic symptoms in clusters
Ipsilateral to side of pain
Ptosis Miosis Lacrimation Conjunctival injection Rhinorrhea Nasal congestion
Horner’s syndrome
Ptosis, miosis, anhidrosis
Common in cluster headaches
Types of cluster headaches
Episodic- most common, 2 cluster periods lasting 7 days to 1 year separated by pain free periods of 1 month or more
Chronic- more than 1 year without remission or with remissions less than 1 month
Probable- fulfilling all but one criteria
Workup of cluster
Unlike other headaches, have to get brain CT or MRI on these patients
Acute cluster traetment
SubQ sumatriptan and oxygen, upright position with 12 L/min 100%
Meds and surgical procedures to prevent cluster HA
Verapamil, Li, steroids and topiramate
Radio frequency, gamma knife, nerve sectioning, cocaine and alcohol
Headache red flags
Progressive HA
Disturbs sleep
Exertional HA
Associated neurologic symptoms, focal deficiency
Fever
Onset of new or different HA
Onset of HA after age of 50
Primary cough HA
HA provoked by coughing or straining in the absence of intracranial disorder
> 40 years old
Primary cough HA features
Sudden
Bilateral
Seconds to 30 minutes
Not associated with NV, photo/phonophobia
Primary cough HA workup
Must do imaging, could have low ICP, IC hypervolemia, carotid artery occlusion, posterior fossa lesion, chiari type 1 malformation, unruptured aneurysm
Imaging primary cough HA
CT or MRI repeated annually for several years
Giant cell arteritis
Chronic vasculitis effecting large and medium sized arteries
Blindness is the worst complication
GCA HA diagnosis
72 years old average, almost never younger than 50
If over 50 and new laterlized HA, abrupt visual disturbance, polymyalgia rheumatica, jaw claudication, fever or anemia, anorexia, weight loss
Diagnostic tests of GCA
Temporal artery biopsy
Halo sign on ultrasound
Elevated ESR
GCA treatment
Start prednisone right away!
HA from intracranial mass lesions
Posterior fossa- occipital HA
Supratentorial lesions- bifrontal HA
Symptoms MAY be nonspecific and variable, worsen with activity and postural change, or have associated NV
Medication overuse headache
Chronic daily headache from someone with a pre existing HA disorder
Addictive personalities, anxiety and fear of HA
MOH most commonly results from overuse of…
Opioids
Butabital containing combo analgesics
ASA/APAP/caffeine combos
MOH criteria
More than 15 days a month
Regular overuse for more than 3 months of:
Ergotamine, Tristan’s, opioids or combo for more than 10 days, or simple analgesics, opioids/ergotamine/triptan combinations greater than 15 days a month
Headache markedly worsened during medication overuse
MOH treatment
Weaning of analgesic overused
Preventive therapy
Avoid abrupt discontinuation
Neuralgia
Neuropathic pain that is paroxysmal, breif, shock like or lightning like
Follows peripheral or cranial nerve distribution
No neuro deficit
Nonpainful stimuli can provoke it
Refractory period following the attack
Trigeminal neuralgia
> 50 years old, women
Vascular compression of trigeminal nerve root
TN definition
Paroxysmal attacks of intense, sharp, superficial stabbing pain in the distribution of one or more branches of the trigeminal nerve, usually unilateral
Facial muscle spasms
One-several seconds and repetitive
Refractory or continuous dull pain
TN triggers
Lightly touching trigger zone Chewing Talking Brushing teeth Cold air Smiling Grimacing
TN diagnostics
CT, MRI, MRA
MRI if trigeminal sensory loss, bilateral, <40 years old
Electrophysiologic trigeminal reflex testing
Jaw jerk reflex
TN prognosis
6-12 months may remit
25-50% stop responding to drug therapy
90% pain free immediately or soon after surgery
Atypical facial pain
Depressed middle aged women
Constant, often burning pain
Restricted distribution, then spreads to face on affected side and sometimes to the opposite side, neck or back of the head
Glossopharyngeal neuralgia
Pain similar to TN
Throat, sometimes deep in ear and back of tongue
Accompanied by syncope sometimes
Glossopharyngeal neuralgia triggers
Swallowing
Chewing
Talking
Yawning
MS?
Postherpetic neuralgia
Pain beyond 4 months from initial onset of herpes zoster
15% of patients with hx of shingles develop this
PHN incidence increases with…
Advanced age
Greater acute pain
Greater rash severity
V1 trigeminal nerve involvement
Neurons vs. neuroglia
Neurons area typical cells within nervous system, info transmitters
Neuroglia are metabolic, immunologic and structural support
Microglia
Activated with immune system and brain injury, clean up cells
Oligodendrocytes and Schwann cells
Oligodendrocytes- myelinate in the CNS
Schwann cells- myelinate in the PNS
Astroctye
Act on blood vessels, are the blood brain barrier
Ependymal cells
Line the ventricles of the brain, produce CSF
Afferent nerve
Arrive in the CNS
Sensation, sensory nerves
Efferent nerves
Exit the CNS, motor nerves
Ascending versus descending tracts
Ascending deliver info to the brain, sensory
Descending deliver info to the periphery, they are motor
If the tract begins with spino…
It is sensory, starts in the spine and goes to the brain
If the tract ends in spinal…
Motor, starts in the brain and ends up in the spine
Posterior column tract is…
A sensory tract
Corticobulbar tract
Motor
Facial expressions, voluntary movement
Extrapyrimadal tracts and symptoms
Info from brainstem to involuntary parts of spine
Dystonia
Akathisia
Parkinsonism
Tardive dyskinesia
Upper motor neuron lesion
Problem with the pyramidal tracts
Loss of the upper motor inhibition allows for exaggerated motor stretch reflex of the lower motor unit
UMN lesion presentation
Spastic paralysis Hyperreflexia Babinski Clonus Clasped knife reflex
LMN lesion presentation
Flaccid paralysis
Atrophy
Fasciculations/fibrillations
Hyporeflexia
LMN lesion examples
Spinal cord injury/nerve root compression Motor neuron disease Peripheral neuropathy Diabetic neuropathy Poliomyelitis
UMN lesion example
Cerebrovascular accident (stroke)
Cervical or thoracic spine injury of the cord
Intracranial tumor
Spasticity
Velocity dependent increase in tonic stretch reflex
Results from abnormal input from dorsal/posterior horn causing the UMN lesion symptoms
Treatment of spasticity
Botox injection
Dorsal rhizotomy
ASIA impairment scale
5 grades from complete, sensory, motor, normal
Glad standard for spinal cord injury
MRI
Spine fx concerning for SCI
Posterior element disruption
Compression fx with posterior wall of vertebral body displaced into spinal canal
Dens fx
SCIWORA
Spinal cord injury without radiographic abnormality
Usually cervical spine
Rare, usually kids under the age of 8
30 min-4 day latent period
Syndromes
5 types, most common in central cord
Treatment of SCI
Stabilize spine and immobilize
High dose IV methylprednisone WITHIN 8 HOURS OF INJURY
Sympathetic autonomic dysreflexia
Sweating
Increased BP
Parasympathetic autonomic dysreflexia
Bradycardia
Autonomic dysreflexia
Occurs with spinal cord lesions above T6
After spinal shock has resolved, around 6 months
More common in quadriplegia
Syringomyelia
Cyst in the spinal cord, destroying a portion of the cord from the inside out
Chiari malformation
Congenital condition, anatomic defect in skull base
Varying degrees of cerebellum and brainstem herniation through foramen magnum
findings in chiari
Pain, numbness, gait ataxia, HA, weakness
Burns from loss of pain sensation, hyperhidrosis, glossy skin, pallor coolness
Charcot joints
Long tract signs
IMPAIRED PAIN AND TEMP WITH PRESERVATION OF LIGHT TOUGH
Delirium
Disorientation, bewilderment, difficulty following commands
Lethargy
Mild drowsiness, aroused by moderate stimuli then drift back to sleep
Obtunded
Moderate drowsiness, sleep more than normal, slow response to stimuli
Stupor
Severe drowsiness, only vigorous and repeated stimuli arouse the individual
Glasgow coma scale
15 is good
<8 intubated
3 is coma
Eyes, verbal, motor
Locked in syndrome
Patient unable to move or speak, but normal cognitive skills
A kinetic mutism
Move or speak very slowly, but are alert
Psychogenic unresponsiveness
Hold eyes closed and resist opening, normal eye responses
Faking a coma
Minimally conscious state
Intact awareness but poor response
Intact wakefulness
Vegetative state
No awareness of self or environment
Intact wakefulness
Brain death
Irreversible and unresponsive coma
Absence of brainstem reflexes
Apnea test- cannot sustain appropriate oxygen level
Traumatic brain injury
Structural or physiologic disruption of brain function
Any period of confusion, disorientation, change in consciousness
Neurologic dysfunction
Basal skull fracture
Hemotympanum
Panda eyes
CSF leakage from ear or nose
Battle sign (behind ear)
Systems effected by dysautonomia
Cardiac GI GU Sexual skin
Postural tachycardia syndrome
Lightheadedness, palpitations, feeling faint
> 30 bpm increase upon standing, no fall in BP
Baroreflex failure
Stress induced systolic BP surges of more than 300, vagus nerve giving no input
Familial dysautonomia
Ashkenazi Jewish descent
Multi system atrophy
Progressive neurodegenerative disorder with autonomic, extrapyrimidal, cerebellar and pyramidal features
Fatal
Autonomic neuropathy
Autonomic dysfunction from postganglionic autonomic nerves
Neruocardiogenic syncope
Symptomatic, sudden drop in BP with simultaneous bradycardia @ 10 minutes
Dysautonomia for tilt table
Continuous drop in BP and no compensatory increase in HR
MS epidemiology
Autoimmune, 20-40 peak incidence
Most common demyelinating disease
Classically… MS
Lesions are separated by space and time
Areas of demyelinating arise, cause problems, and slowly resolve
MS mechanism of disease
Demyelination occur
Microglia activation increases tissue damage
Lesions re-myelinate with time