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a neurological examination involves::
• Mental Status
• Cranial Nerves
• Motor Examination
• Sensory Examinaton
• Coordination
• Gait
mental status involves:
Level of consciousness/alertness
Attention
Memory
Language
Calculations and visuao-spatial tasks
what are some ways to test attention?
Serial sevens, digit span, “world” backwards
what does language involve?
fluency, comprehension, naming, repetition, reading, aphasia
what are types of memory?
Recent vs. remote memory
Anterograde vs. retrograde amnesia
what are types of aphasia?
receptive (Wernicke’s) - temporal lobe
can’t understand
expressive (Broca’s) - frontal lobe
global
mix of both receptive and expressive
conduction
comprehension intact but trouble with repetition
calculations and visu-spatial tasks involve:
– Simple calculations
– Right/left discrimination
– Finger indentification
– Reading/writing ability
– Copying shapes/geometric figures
– Gnosis
which lobe is responsible for calculations and visuo-spatial tasks?
parietal lobe
how can frontal lobe be tested?
clock drawing test
sequencing tasks
set switching
frontal release signs
what are frontal release signs?
exists in newborns and usually goes away but in pts with frontal lobe deficits, these reflexes may come back
grasp
paratonia (resistance in limbs)
palmomental (twitch on palm)
glabellar (unable to suppress blink reflex)
what is the clinical relevance of CN I (olfactory)?
– Head/Facial Trauma
– Frontal lobe masses
– Parkinson’s Disease (loss of smell can be first sign)
– Epilepsy
t/f: when testing CN I, it is important to use pleasant smells because noxious odors can stimulate the trigeminal nerve.
true
what are monocular visual defects?
primary ocular disease (retinal disease, glaucoma)
anterior to optic chiasm
what are binocular visual defects?
optic chiasm
posterior to optic chiasm
occipital cortex
when performing a pupillary light reflex exam, what 2 things should we look for?
direct
consensual
an optic nerve lesion leads to loss of direct and consensual responses
CN III (oculomotor) is located where?
midbrain
eyelid opening is controlled by what muscle?
levator palpebrae
extrinsic deficit of the oculomotor n CN III will show what clinical presentation?
eye deviation “down and out”
pupil fixed and dilated
intrinsic deficit of the oculomotor n CN III will show what clinical presentation?
eye deviation
spares pupil
pupillary constriction is controlled by S/PS pathway
PS
trochlear n (CN IV) is located where
midbrain
deficits to the trochlear n. (CN IV) presents as
– Vertical diplopia (double vision)
– Hypertropia (eye deviates upward)
– Often there is a head tilt, usually towards opposite side of lesion
abducens n (CN VI) is located where
pons
deficit to the abducens n (CN VI) presents as
eye deviated medially, limited abduction of ipselateral eye
deficits to the trigeminal n (CN V) presents as
facial sensory loss (anterior to ear)
jaw deviation ipsilateral to lesion
deficits to the facial n (CN VII) presents as
– Peripheral facial weakness (eyelid as well as mouth)
– Taste loss ipsilateral to lesion
– Hyperacusis ipsilateral to lesion
deficits to the vestibulocochlear n (CN VIII) presents as
Lesions lead to sensory hearing loss and (peripheral) vertigo
deficits to the glossopharyngeal (IX) and vagus (X) presents as
– Dysarthria/dysphagia
– Inability to elevate palate (contralateral uvulal deviation)
deficits to the hypoglossal n (CN XII) presents as
Lesions lead to ipsilateral tongue deviation
Pupillary reflexes are linked to which CNs?
II
oculocephalic reflexes are linked to which CNs?
III, VI, VIII
“doll’s eyes'“ - move pts head side to side but eyes should stay staring straight ahead
vestibulo-ocular reflexes are linked to which CNs?
III, VI, VIII
– Cold water injected into ear canal
– Eyes deviate towards injected side
– Nystagmus (fast beating) to opposite side
corneal reflexes are linked to which CNs?
V, VII
gag reflexes are linked to which CNs?
IX, X
motor exams should involve:
bulk and tone
strength
reflexes
Babinski/Hoffman
how is strength graded on a motor exam?
scale 0-5
hypotonia, fascilations, and atrophy are signs of…?
LMN weakness (bulk and tone exam)
spasticity, lack of atrophy are signs of…?
UMN weakness (arm tends to be flexed, leg extended during bulk and tone exam)
how are reflexes graded on a motor exam?
scale 0-4
0: areflexic
4+: clonus
dorsal column pathways
where does it cross? what are the sensory modalaties?
– Crosses at medulla
– Light Touch
– Proprioception/Vibration
spinothalamic pathways
where does it cross? what are the sensory modalaties?
– Crosses in spinal cord
– Pain (pin prick)
– Temperature
coordination exams primarily assesses which lobe function?
cerebellum
what are some coordination exams and signs of deficit?
• Finger-to-nose/Heel-to-Shin
– Dysmetria
– Intention tremor
• Rapid Alternating Movements
• Mirror movements
how can we test gait?
station/balance
getting up from chair
pull test
Romberg test (closed eyes) to assess dorsal column pathway, not cerebellar function
propulsion
stride length, arm-swing
speed
turning
heel/toe/tandem gait
what are some abnormal gaits?
ataxic (wide base)
spastic hemiplegic gait (children)
parkinsonian gait (tremor in hand, diminished arm swing)
when taking a history of someone with headaches/facial pain, what is important to collect?
– Acuity of onset
– Duration to maximal severity/Pain Scale
– Quality of pain (Pressure, squeezing, pounding, throbbing, stabbing)
– Distribution of pain
– Triggers
– Relieving/exacerbating factors
“Thunderclap” Headache is a red flag symptom of…?
Ruptured aneurysm
positional component Headache is a red flag symptom of…?
intracranial pressure
Headache on awakening is a red flag symptom of…?
mass lesion, elevated pressure
focal neurological signs is a red flag symptom of…?
mass lesion, dissection
neck rigidity is a red flag symptom of…?
meningeal irritation
new Headache in elderly patient is a red flag symptom of…?
temporal arteritis
what is the most common headache type?
tension headaches
characteristics of tension headaches
• Lifetime prevalence of 69% in men, 88% in women
• “dull”, “pressure”, “squeezing”
• Usually bilateral but can be unilateral
• Non-pulsatile
• Can have photophobia but usually no nausea
• No aura
what are the types of migraines?
Migraine without aura (“Common”)
Migraine with aura (“Classic”)
Hemiplegic Migraine (“Complicated”)
Status Migrainosis
what is common in patients with migraines?
family history
characteristics of migraines
About 18% of women, 6% of men
– Unilateral location
– Pulsating quality
– Moderate to severe pain “8/10”
– Avoidance of routine physical activity
– Duration: 4-72 hours if untreated
what are some associated features with migraines?
Nausea/vomiting
Photophobia/phonophobia
Triggers
Foods: preservatives, MSG, chocolate, cheese, alcohol
Poor sleep
Other environmental (smells, lights)
childhood migraine variants include:
cyclic vomiting
abdominal pain, “colic”
characteristics of migraine with aura
– No motor weakness
– at least one of the following:
• reversible visual symptoms
• reversible sensory symptoms
• reversible dysphasic speech disturbance
• vertigo
• each symptom lasts ≥5 and ≤60 minutes
characteristics of hemiplegic migraine
• Motor weakness also part of aura
• Aura otherwise the same
• Diagnosis of exclusion
characteristics of cluster headaches
Uncommon
Men > Women (4-5 to 1)
Features:
Unilateral, excruciating pounding/penetrating pain
Peri-orbital, temporal, scalp, maxilla
Autonomic features
Ptosis, lacrimination
Come in clusters with periods of remission
who is the classic cluster headache patient?
male, 40’s, heavy drinker/smoker
what are treatments for migraines?
Abortive
– NSAID’s
– Triptans (avoid in hemiplegic migraine)
– Muscle relaxants (tension)
– Anti-emetics (migraine)
– Corticosteroids
– Oxygen (cluster)
what migraine treatment should be avoided in hemiplegic migraine?
triptans
what should be avoided in migraine treatment?
avoid analgesic rebound (tolerance buildup, take more and more drugs)
if at least 2 days of headache a month, what treatments can be considered?
Tricyclic antidepressants
amitriptyline, nortriptyline
Beta blockers (non-selective)
propranolol
Calcium channel blockers
verapamil
Antiepileptics
Topiramate, valproic acid
Botulinum Toxin
what is trigeminal neuralgia?
Paroxysmal attacks of pain lasting from a fraction of a second to 2 minutes, affecting one or more divisions of the trigeminal nerve
V2, V3 more common
V1 relatively rare
pain from trigeminal neuralgia has at least 1 of what characteristics?
– intense, sharp, superficial or stabbing
– precipitated from trigger areas or by trigger factors
t/f: in trigeminal neuralgia, there is no clinically evident neurological deficit and is not attributed to any other disorder
true
what treatment options are there for trigeminal neuralgia?
Antiepileptics
carbamazepine, oxcarbazepine, phenytoin
gabapentin
Muscle relaxants
Baclofen
Surgical
Rhizotomy
Microvascular decompression
Gamma knife
what are the types of movement disorders?
tremor: rhythmic, oscillatory, across a fixed axis
chorea: random, irregular
myoclonus: rapid, jerk-like movements
dystonia: sustained contractions
tics: semi-voluntary, stereotyped
tardive dyskinesia is due to…?
chronic dopamine antagonist use
– Antipsychotics
– Anti-emetics
charceristics of tardive dysinesia?
hyperkinetic movements
choreic movements most common (esp orofacial, buccolingual distribution)
dystonia, tics
what is the pathophysiology behind tardive dyskinesia?
pathophysiology unclear (dopamine receptor hypersensitivity)
what are treatment options for tardive dyskinesia?
– Stop offending medication
– Dopamine blocking agents
– Benzodiazepines
– VMAT2 inhibitors (dopamine depleters like Tetrabenazine, deutetrabenazine, valbenazine)
– Botulinum toxin (if dystonic)
what is a common tic disorder?
Tourette’s Syndrome
characteristics of Tourette’s syndrome?
common (1% of population)
childhood onset (7 yo average)
motor and vocal tics
what are some neurobehavioral symptoms of Tourett’es syndrome?
– Attention deficit disorder
– Obsessive compulsive behaviors
– Learning disabilities
what are treatment options for Tourette’s syndrome?
– Tics: dopamine blockers/depleters
– Behavioral: clonidine, methylphenidate, SSRI’s
what muscles do hemifacial spasms affect?
Myoclonus/dystonia of facial muscles
– Orbicularis oculi/eyelids (blepharospasm)
– Lower face
hemifacial spasms are caused by…?
Idiopathic or structural/compressive lesion involving facial nerve
– Vascular
– Mass
– Demyelinating lesion (MS)
what are treatment options for hemifacial spasms?
responds to botulinum toxin injections
what is palatal myoclonus?
A involuntary, rhythmic movement of the palate (Persists in sleep)
what is palatal myoclonus caused by?
– Brainstem lesion involving triangle of Guillain-Mollaret (Red nucleus, inferior olivary nuclues, dentate nucleus)
– Idiopathic
what are treatment options for palatal myoclonus?
– Clonazepam
– Valproic acid
– Carbamazepine
– Botulinum toxin