Neurology Flashcards
Two types of injuries for TBI
EX of both
PRIMARY: direct result of initial trauma–gross result
EX–fx, cerebral contusion, vascular disruption
SECONDARY: results from the evolution of the initial injury or complications, damage on a molecular level—-what we aim to minimize
EX: hypoxia, ischemia, cerebral edema, IntracranialHTN
Cushings triad
- hypertension
- bradycardia
- irregular respirations
CCP=
cerebral perfusion pressure=MAP-ICP
normal CPP
b/w 70 and 90 mmHg
list the primary HA
- tension
- migrane w/ or w/o aura
- cluster
What is a secondary HA
-list the examples
-account for small percent of HA
-sequelae of another disease process (EX: incr ICP)
EX:
-SAH
-ICH from tumor, trauma or idiopathic
-hypertensive crisis
-acute glaucoma
-sinus infection
-TMJ
-temporal arteritis
-meningitis
MC HA?
PRIMARY—90%
HA caused by?
traction, displacement and inflammation or distention of the pain-sensitive structures in head or neck
Head HX questions: H E A D
H:
- how severe is your headache scale 1-10
- how did this HA start–gradual, sudden,
- how long have you had this HA
E:
- ever had HA before?
- ever had a HA this bad before?
- ever have HA like this one in the past?
A:
- any other s/s before or during HA?
- any other s/s right now?
D:
- desc the quality of pain
- desc location of pain
- desc where pain radiates
- desc any other medical problems
- desc your use of meds
- desc any hx of trauma or medical or dental procedurs
HA differentials by time course: list the HA for each timeline
- Acute onset
- Subacute onset
- Chronic
- SAH, carotid/vertebral dissection, meningitis or encephalitis, glaucoma, acute iritis
* less common: lumbar puncutre, HTN encephalopathy, coitus - Giant cell (temporal) arteritis, intracranial mass (tumor, subdural hematoma), trigeminal neuralgia,
- migraine, med overuse, cluster, tension, cervical spine disease, sinusitis, dental disease
List the HA red flag S/S
- thunderclap onset
- worsens with coughing, sneezing, straining, worse at night,
- increasing in frequency
- new HA in 50+ with no HX
- New HA in CA PT
- HA+ Fever
- new HA in immunocomp PT
- HA + focal neruologic signs
- HA + Seizures
what disease processes can cause Thunderclap HA
VASCULAR PATHOPHYSIOLOGY
- intracranial hem (SAH)
- HTN emergency
- venous sinus thrombosis
- Cervical artery dissection
- pituitary apoplexy
HA worse at night, worse with coughing/sneezing/straining/
or
increasing in severity
ELEVATED ICP
- tumor
- hydrocephalus
- idiopathic intracranial HTN
New HA in older adult 50+ w/ no prior hx
MASS LESION INFLAMMATION DISEASE:
- tumor
- giant cell arteritis
- primary CNS vasculitis
New HA in PT with hx of CA
…what do we think of?
METASTASIS
new HA in immunocomp PT
OPPORTUNISTIC INFECTION
- toxoplasmosis
- primary CNS lymphoma
- cryptococcal (fungal) meningitis
HA + fever
INFECTION
- meningitis
- cerebral abscess
HA + seizures
FOCAL LESION
- tumor
- infection
- hemorrhage
HA + focal neuro signs
FOCAL LESION
- tumor
- infection
- hemorrhage
- ischemic stroke
Which HA is MC in women
tension and migraine
main differences b/w s/s of:
-tension vs migrane w/o aura HA
tension: nonpulsatile, dull pain, bilateral, no n/v photophobia or phonophobia, s/s not worsen w/ activity
migraine: pulsatile, unilateral, YES: n/v, photophobia and phonophobia, s/s worsen with activity
list the 5 prophylactic drug therapies to prevent/reduce freq of migraine HA
- BB–propranolol
- CCBs–verapamil
- TCAs–amitriptyline
- anticonvulsants–valporic acid and topiramate
Indications for Head CT w/ HA
- prior to LP
- abnorm neuro exam
- ams
- abnm fundoscopic exam
- meningieal signs - Emergent–conduct prior to leaving office/ED
- abnm neuro exam
- ams
- thunderclap HA - Urgent–scheudled prior to leaving office/ED
- HIV pos PT (MRI is preferred)
- age 50+ with normal neuro exam
MC aura
VISUAL
-scotomata—flashing lights
Name the classic CSF findings for:
- MS
- Guillain Barre
- Bac Meningitis
- Viral meningitis
- Fungal or TB meningitis
- Idiopathic intracranial HTN
- SAH
- High IGG (oligoclonal bands)
- High protein with normal WBC count
- High protein, incr WBC (polymorphonuclear neuts) and decr glucose
- Normal glucose, incr WBC (lymphocytes)
- Decr glucose, increase WBCs (lymphocytes)
- incr CSF pressure otherwise normal findings
- Xanthochromia, blood in CSF
younger PT diagnosed with Trigeminal neuralgia.. what do we want to r/o or be suspicious of?
Multiple sclerosis
cranial nerve palsy and can technically be classed as a LMN disorder?
Bell’s Palsy
first line tx for abortive care of acute migraine
NSAIDS**** or acetominophen or Excederin
first line tx for acute tension HA
NSAIDs ** + local heat
or
other analgesics
first line tx for acute cluster HA
100% oxygen
and
SQ Sumatriptan
1st line for cluster HA prophylaxsis
Verapamil
First line tx for Pseudotumor cerebral aka idiopathic intracranial HTN?
Acetazolamide (diuretic) + wt loss
*can use furosemide as adjunct
First line tx for trigeminal neuralgia
Carbamazepine PO —anticonvulsant
If Bell’s palsy is caught in the first 72 hours, what is FL tx?
-Prednisone
or
acyclovir+Prednisone (glucocorticos)
what is the MC type of intracranial hem caused by a ruptured cerebral aneurysm?
SAH
or
intracerebral hemorrhage
Intracranial hemorrhages divided into two classes:
-list what is in each class
- Extra-axial hemorrhage–occurs outside the brain tissue
- epidural
- subdural
- subarachnoid - Intra-axial hemorrhage–occurs inside brain tissue
- intracerebral hemorrhage (aka hemorrhagic stroke)
what causes a subarachnoid hemm?
-cerebral aneurysm rupture
another term for intracerebral hemorrhage?
hemorrhagic stroke
Hemorrhagic strokes are often secondary to?
HTN
two types of weakened BVs can cause hemorrhagic stroke
- aneurysms
- AV malformations
Ischemic strokes: three (two mainly) types defined and which is more common
Thrombotic stroke (2/3)–caused by blood clot that develops in the BVs inside brain
-Embolic (1/3)–caused by blood clot or plaque debris that develops elsewhere in the body–then travels to one of BVs in brain via blood stream (AFIB is COMMON)
third: hypoxia… hypotension and poor cerebral perfusion… border zone infarcts…there is no vascular occlusion but can lead to infarcted areas
* concept for watershed infarct**
Stroke s/s are ipsilateral or contralateral to the part of the brain affected?
contralateral (side of the body with s/s is opposite side of brain affected)
- right sided s/s=left side stroke
- left sided s/s=right side stroke
Define TIA
TRANSIENT ISCHEMIC ATTACK
-neuro deficits w/o acute infarct that lasts >24 hours
Four main “types” of intracranial hemorrhages
*which can be classified under hemorrhagic stroke?
Bleeding inside the brain
- epidural
- subdural
- subarachnoid
- intracerebral hem
***last two can also be classified under hemorrhagic stroke
where is the bleeding in a epidural hematoma?
space b/w skull and dura
MCC of epidural hematoma
middle meningeal artery rupture
*assoc w/ temporal bone fracture
define hemiparesis
muscle weakness or partial paralysis on one side
*also called hemiplegia
Uncal herniation
- define
- can develop secondary to?
CNIII palsy... ipsilateral eye of injury is: -fixed -dilated -blown CAN DEVELOP DUE TO: -epidural hematoma
on CT, does the epidural hematoma cross suture lines?
NO
CT RESULTS: biconvex “lens shape” hyperdense in temporal area
epidural hematoma
First line tx for epidural hematoma
hematoma evacuation
OR
craniotomy
MCC of subdural hematoma
rupture of cortical bridging VEINS
post blunt force trauma
subdural hematoma is bleeding where
space b/w dura and arachnoid membranes
**bridging veins rupture
CT: concave/crescent shape bleed that does cross suture lines
Subdural Hematoma
First line tx for subdural hematoma
- if PT is stable and CT doesnt show signs of herniation (midline shift <5mm)… OBSERVE
- +s/s of incr ICP or midline shift is >5mm…. SURGERY
- burr hole trephination
- surgical evacuation
- decompression craniotomy
Subarahchnoid hemorrhage is where
space b/w arachnoid membrane and pia mater
MCC of subarachnoid hem?
-other commmon cause
rupture saccular (berry) aneurysm —75% cases for nontraumatic
other:
- trauma
- AV malformations
mortality rate for nontraumatic SAH
50%
thunderclap HA
SAH
Xanthochromic CSF results?
SAH
*CSF is yellow to pink
TX options for SAH
- BEDREST*
- Nimodipine to reduce cerebral vasospasms
- Labetalol to lower BP
- surgical coiling or clipping
MCC overall for intracerebral hem?
second MCC?
HTN from angiopathy from systemic HTN–number one
Cerebral amyloid angiopathy (disease of BV)
MCC for intracerebral hem in:
- eldery?
- kids?
elderly–> cerebral amyloid angiopathy
kids–>AV malformation
with intracerebral hem, how do we want to lower BP?
GRADUALLY
IV BBs or CCBS or hydralazine
- labetalol
- nicardipine
tx for intracerebral hem
SUPPORTIVE
-gradual BP reduction
Reduce ICP and prevent incr ICP
- raising bed 30 degrees
- limit IV fluids
- BP management
- Analgesia
- sedation
what is the 3rd MCC of death in the US?
Cerebrovascular accident—stroke
hemorrhagic stroke–another name for it?
intracerebral hemorrhage
two types of hemorrhagic stroke
- intracerebral hem
- SAH
bulging weakened area in the wall of an artery in brain
- what is it?
- what does it result in?
CEREBRAL ANEURYSM
- can result in abnormal widening or ballooning
- weak spot=risk for rupture/bursting
which BV layer is affected in cerebral aneurysm?
muscular layer of the artery wall is thin….
-so instead of three layers, now the BV only has two
which arteries in the brain can develop an aneurysm?
mc where
ANY OF THEM
MC in the front part of brain
MC type of aneurysm
Berry or saccular aneurysm
80-90%
when are cerebral aneurysms diagnosed?
usually not diagnosed until they rupture….
but sometimes PT can have s/s before rupture.. and then aneurysm will be dx on CT
S/S of a cerebral aneurysm
-that did not rupture
If large enough, will cause: HA or pain behind or near one eye vision deficits eye movement deficits **can cause s/s if its pressing on adjacent structure.. like eye or nerves OR cause s/s from tiny leaks
MC initial symptom of a cerebral aneurysm?
if it RUPTURED
- sudden/thunderclap HA
- SAH
s/s of SAH
worst HA of my life stiff neck/nuchal rigidity n/v changes in mental status----like drowsiness dilated pupils \+LOC loss of coordination photophobia coma death
how to diagnose Cerebral aneurysm
*gold standard?
CT scan WITH contrast ****
MRI
GOLD STANDARD–angiography
*but dont start with that.. usually start with CT
where is berry aneurysm located
-where on arteries does it form?
in the circle of willis
-anterior communicating artery–MC
forms at the “Y” segment or bifurcation of arteries and branches of large arteries at base of brain…. aka circle of willis
RF for cerebral aneurysm
smoking
htn
hypercholesteremia
ETOH
Herald bleed
cerebral aneurysm leak
- 40% in PTs
- less severe but atypical HA
- focal neuro s/s from pressure on brain or CNs
- occur 1-3 weeks prior to severe SAH
TX for cerebral aneurysm
surgery
-clipping or coiling
what is brain arteriovenous malformation
-cause?
tangle of abnormal BVs
-connecting arteries and veins
- rare
- idiopathic.. most ppl are born with them
s/s of AVM
asympto usually—until rupture–about 1/2 of cases are asympto until rupture
w/o hemorrhage s/s:
- seizures–>usually partial seizures (11-13%)
- acute hemiparesis/muscle weakness one side and other focal neuro deficits
- HA (0.2%)
in about 1/2 of PTs with AVM.. what is the first sign?
intracranial hemorrhage!
gold standard for AVM diagnosis, tx plannning, and follow-up after tx
angiography
what is the most dangerous congenital vascular malformation and why?
AVM
- potential to cause intracerebral hem and epilepsy
- AVM will grow as PT gets older
usual presenting age for AVM
10-40
RF for AVM
male
fam hx
Complications with AVM
- hemorrhage
- reduced o2 to brain–blood rushes quickly through AVM–moves so fast that some brain tissue not oxygenated
- Brain damage–as body grows, the AVM grows bc it recruits more arteries to supply blood–growing AVM eventually displaces or compresses part of brain
do we see midline shift with large AVMs?
no, because AVM is SLOW growing.. so the brain has time to adjust and move around without being pushed
diagnostic tests for AVM
CT WITH Contrast
MRI/MRA
cerebral angiography
TX for AVM
main goal of tx is to prevent hemorrhage **
- surgical resection of tangled mass
- endovascular emoblization that blocks feeding arteries to AVM
ruptured AVM can cause….
- strokes (1-2% of all)
- cause 3% of strokes in young adults
- cause 9% of all SAH
what is TIA
transient ischemic attack
how long does TIA usually last
complete resolution of s/s?
no more than 24 hours
can be as little as few minutes
*resolution of s/s: within 1 hour
TIA of ophthalmic artery?
Amaurosis fugax
which artery is affected in amaurosis fugax?
TIA in the internal carotid
what is test of choice for definitive TIA?
conventional angio
with TIA, do we want to lower the BP?
NO!
unless it is >220/120
what is contraindicated in management of TIA
thrombolytics
first line tx for noncardiogenic TIA
ANTIPLATELET TX:
ASA***
clopidogrel
Percent of stroke after TIA?
30% risk within 5 years of TIA
ABCD2 Score Assessment
- TIA
- assesses risk of stroke w/in 3-90 days post stroke
- **highest risk for stroke is days after TIA
- PT gets one pt for each of the following:
A: age>60
B: BP >140/90
C: Clinical s/s (one PT for slurred speech and two PTs for unilateral weakness)
D: Duration (one PT for >10 mins and 2 points for >60mins)
D: diabetes
when do we allow permissive HTN and why?
with TIA and ischemic stroke PT
*bc their brain is used to having higher pressure, so if we drop it too fast, perfusion drops as well
**hemm stroke we want to drop the BP
ABCD2 scoring
0-3points=?
4-5 points=?
6-7points=?
0-3= 3.1% 90 day stroke
4-5= 9.8% 90 day stroke
6-7= 17.8% 90 day stroke
most modifiable and significant RF for stroke
HTN
aphasia
diff speaking or understnad speech
apraxia
inability to perform purposive actions
ataxia
loss of full control of bodily movements
with ischemic stroke, why can the CT be normal w/in first 24 hours?
bc it takes 24 hours for brain tissue death to show on CT
most accurate diagnostic test to diagnose stroke?
MRI
best initial diagnostic test for stroke?
CT w/o contrast
immediate tx for ischemic stroke?
allteplase
contras for alteplace?
BP 185/110 or higher;
recent bleeding;
bleeding disorder,
recent trauma.
can give alteplase how long after intial s/s of stroke
3
who can get thrombolytic tx for ischemic stroke up to 4.5 hours??
-less than 80 YO
<25 on NIH stroke scale
no DM with previous stroke
when is mechanical thrombectomy indicated?
within 24 hours of s/s onset
for large artery occlusion in anterior circulation
long term management ischemic stroke
- antiplatelet therapy: ASA, clopidogrel or dipyridamole
* not started until 24 hours after Alteplace* - Statin therapy regardless of their LDL
If PT is already on ASA prior to stroke… what is the long-term mangement plan?
either add on Dipryidamole or switch to clopidogrel
when to lower BP with ischemic stroke
if BP is over 185/110 and thrombolytics are to be administered
OR
BP over 220/120 and no plan to use thrombolytics
lacunar stroke?
-locations
small lesions that are under 5mm in diameter that occur in short penetrating (tiny arteries) arteries of
- basal g
- pins
- cerebellum
- internal capsule
- thalamus
- deep cerebral white matter
DEEP STRUCTURES*
diff b/w ischemic stroke and lacunar stroke
LACUNAR: in the tiny tiny vessels deep in brain
ISCHEMIC: larger vessels
TX for lacunar stroke
ASA and RF modifications
***no anticoagulation indicated **
CT shows: small, punched-out hypodense areas?
Lacunar Stroke
dysarthria
slurred speech
MC presenting s/s for lacunar stroke?
dysarthria with clumsy hand (clumsy hand syndrome)
-PURE motor or PURE sensory deficits can be seen too
classic territory for watershed infarct
between MCA and ACA
or
MCA and PCA
typical pathway for movement
primary motor cortex–brainstem–spinal cord—nerves—innvervate skel muscles
two main motor function categories
Upper motor neurons
lower motor neurons
decussation area
corticospinal tract
-area where motor nerves “switch” to the opposite side of body
why person who has stroke on L side has R sided s/s**
Upper motor neurons run from……
primary motor cortex down to the VENTRAL (anterior) horn of SC via corticospinal or pyramidal tract
what tract does UMNs run on?
corticospinal or pyramidal tract
what tract do the UMNs innervating cranial nerves run on?
corticobulbar tract
Pthway for UMNs innervating CNs
primary motor cortex–cranial nerve nuclei–brainstem
*corticobulbar tract
Lower motor neurons run from…
VENTRAL (anterior) horn of SC to the target muscle
LMNs innervating the head and shoulders are found
in the CNs
usual complaints from PTs with motor deficits
weakness heaviness stiffness clumsiness impaired muscle control diff executing movements
during PE of patients with motor complaints, what is something very imp to look at?
the MUSCLE appearance -wasting? -atrophy? -spasm?
tone muscle power cordinationg reflexes gait
Monoplegia/monoparesis
paralysis or severe weakness of muscles in one limb
hemiplegia/hemiparesis
weakness/paralysis in both limbs (and something the face) on one side of the body
paraplegia/paraparesis
weakness/paralysis of both LEGS
quadriplegia/quadriparesis
weakness/paralysis of all four limbs
term for paralysis or severe weakness of muscles in one limb
monoplegia or monoparesis
term for weakness/paralysis in both limbs (and something the face) on one side of the body
hemiplegia/hemiparesis
term for weakness/paralysis of both LEGS
paraplegia paraparesis
term for weakness/paralysis of all four limbs
quadriplegia or quadriparesis
S/S of UMN lesion
weakness or paralysis
- hypertonia/spasticity
- incr tendon reflexes
- extensor plantar (babinski) response
- loss of superficial adbominal reflexes
- little if any muscle atrophy
weakness or paralysis
- hypertonia/spasticity
- incr tendon reflexes
- extensor plantar (babinski) response
- loss of superficial adbominal reflexes
- little if any muscle atrophy
S/S of UMN lesion
S/S of LMN lesion
weakness or paralysis *wasting and fasciculations or invovled muscles *hypotonia or flaccidity *loss of tendon reflexes normal abdominal and plantar reflexes little if any muscle atrophy
weakness or paralysis *wasting and fasciculations or invovled muscles *hypotonia or flaccidity *loss of tendon reflexes normal abdominal and plantar reflexes little if any muscle atrophy
LMN lesion s/s
motor neuron disorders are character by degeneration of…….
anterior horn cells in SC**, motor nuclei of lower cranial nerves in the brain stem and corticospinal and corticobulbar pathways
list the motor disordes
ALS polio MS tetanus GBS Myasthenia gravis
list the movement disorders
tremors essential (familial) tremor tics Gilles de la tourette syndrome parkinson
invol rhythmic oscillation of one or more body parts. May occur at rest, posture, and action and can be part of the cerebellar syndrome
tremor
define tremor
invol rhythmic oscillation of one or more body parts. May occur at rest, posture, and action and can be part of the cerebellar syndrome
irreg random rapid low amplitude semi-purposelful dance-like movements
chorea
define chorea
irreg random rapid low amplitude semi-purposelful dance-like movements
simultaneous contractions of agonsit and anatagonist muscles causing patterned sustained postures and irregular repetitive movements
dystonia
define dystonia
simultaneous contractions of agonsit and anatagonist muscles causing patterned sustained postures and irregular repetitive movements
sudden lightening like random jerks or sudden inhibition of on-going muscle activity
myoclonus
define myoclonus
sudden lightening like random jerks or sudden inhibition of on-going muscle activity
constellation of hyopkinetic symptoms such as bradykinesia, rigidity, postural instability and resting tremor
parkinson
motor activity as a voluntary effort to relieve uncomfortable sensations
akathisia
define akathisia
motor activity as a voluntary effort to relieve uncomfortable sensations
Parkinson tremor:
- distribution
- what makes it worse and better
- body part affected
- writing?
- progressive or sudden
- fam hx
- other neuro s/s with it
- drugs that help
tremor present at rest “rolling pill”.. increases with walking and decreases with posture holding or action
asymmetric distribution
hands and legs usually affected
small and illegibile writing
progresive course
less common hx in fam
other s/s–bradykinesia, rigidity, loss of postural reflxes
drugs that make it better–levodopa, anticholinergics
Essential tremor:
- distribution
- what makes it worse and better
- body part affected
- writing?
- progressive or sudden
- fam hx
- other neuro s/s with it
- drugs that help
posture holding or action increases
symmetric distrib
hands, head, voice distrib
tremulous writing seen
stable or slowly progressive
often related to fam hx
no other s/s seen with it
drugs that make better: ETOH, propranolol and primidone
ALS is neurodegeneration of what
anterior horn cells
why sensation is not affected
ALS affected LMN or UMN?
BOTH
*why it causes progressive motor dysfunction
CM for ALS
- asymmetric limb weakness (MC presenting symp)
- bulbar symptoms: diff chewing, dysphagia, dysarthria, aspiration
- cognitive impairment–frontotemporal dysfunction
MC presenitng symp for ALS
asymmetric limb weakness
“bulbar” symptoms means
muscles that control swallowing, speaking, chewing etc
- diff in:
- chewing
- swallowing
- speech
- aspiration
what functions are spared with ALS
sensory
voluntary eye movement
spinchter control
sexual function
PE findings for ALS
mix of UMN and LMN s/s is hallmark
UMN:
- muscle stiffness
- hyperreflexia
- spasticity
- weakness
LMN:
- muscle atrophy
- hyporeflexia
- muscle contractions/fasciculations
diagnose ALS?
results?
electromyography–shows loss of neural improvement and reinnervation in muscle groups
electromyography results–shows loss of neural improvement and reinnervation in muscle groups
ALS
Management for ALS
- Riluzole–reduces glutamate accumulation in neurons
* *only known drug to impact ALS by reducing progression up to six MOs - Edaravone–free radical scavenger that helps in early-stage disease
- symptom managment:
- drooling: muscarinic anticholinergic drugs
- braces/walkers/wheelchairs
- diet–usually progresses to liquid diet…. then progresses to tube feedings bc of dysphagia
- ventilation– towards the end of disease
What is the MC cause of death for ALS?
respiratory failure
prognosis for ALS
fatal w/in 3-5 years of diagnosis
**resp failure MC cause of death
what are some of the MC presenting s/s of MS?
sudden blurred vision with -decreased acuity or -double vision -paresthesias (numbness/tingling) in extremities, ataxia, fatigue and focal motor s/s *trigeminal neuralgia \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *sensory loss *optic neuritis *weakness *fatigue ** *paresthesias
what is MS
autoinflammatory disease causing
- demyelination
- neuronal loss
- scarring within white matter of brain + SC
what is commonly seen with MS/typical complaint
visual disturbances over many yrs
PT demographic we think of for MS
WOMEN and young adults 20-40 YO
three types of MS
*MC?
- relapsing-remitting disease (MC..85%)–episodic exacerbations
- Progressive disease–progressive decline w/o acute exacerbations
- Secondary progressive–relapsing/remittent that becomes progressive
prevalence of MS rises with ?
- increasing distance from equator
* vit d may play a role?
patho of MS
focal and scattered areas of demyelination
-triggered by immune response directed against myelin self-antigens
clinical manifestation for MS
initally— the sudden blurry vision or double vision or loss of vision
sensory disturbances: pain, parathesias weakness motor deficits--gait and balance problems -fatigue -SC s/s--bladder or bowel dysfunction
Uhthoff’s phenomenon–what is it ?
seen with?
Seen with MS
*worsening s/s with heat –excerise, fever, hot tubs, weather
PE findings for MS
- UMN–hypertonia and hyperreflexia and spasticity along with upward babinski sign
- Lhermitte’s sign–neck flexion causes lightening shock pain rad down to spine and legs
- cerebellar–Charcot’s neurologic triad: nystagmus, staccato speech, intentional tremor
- optic neuritis with Marcus-Gunn pupil
- Internuclear opthalmoplegia–inability to adduct eye on the side of lesioin w/ nystagmus in the other eye
SC s/s–bladder, bowel or sexual dysfunction
what is -Lhermitte’s sign
seen with?
- -neck flexion causes lightening shock pain rad down to spine and legs
- seen with MS
what is Charcot’s neurologic triad and seen with what disease
: nystagmus, staccato speech, intentional tremor
MS!
Marcus-Gunn pupil.. what is it
seen with?
pos swinging light test
MS!!!
what is -Internuclear opthalmoplegia and what is it seen with
–inability to adduct eye on the side of lesioin w/ nystagmus in the other eye
MS
PE: UMN s/s, Lhermitte’s sign, Charcot’s neurologic triad, optic neuritis with Marcus-Gunn pupil, Internuclear opthalmoplegia and SC s/s
MS
is MS autoimmune?
YES
what is a strong sign of MS
internuclear ophthalmpleiga
-inability to adduct the eye on side of lesion w/ nystagmus on the other eye
life expectancy for MS?
near normal
major long term problem with MS?
optic neuritis
CSF in MS shows–
increased IGG
oligoclonal bands
myelin fragments
CSF shows increased IGG
oligoclonal bands
myelin fragments
what disease
MS
cerebellar involvement in MS is manifested by?
tremors ataxia babinski sign nystagmus staccato speech
how do we diagnose ms
mainly clinical
*MRI with gadolinium—BEST INITIAL TEST most accurate too
LP
hallmark findings on MRI with MS
hyperintense white matter plaques
MRI shows hyperintense white matter plaques
MS
Oligoclonal bands in csf indicates?
MS
Management for acute episode of MS?
FIRST LINE–IV glucocorticos high dose
2nd–plasmapheresis if not responsive to glucos
Managment for prevention of relapse and progression of MS?
1st line–Beta Interferon (anti-inflamm) or Glatiramer (immunodilators)
2nd–Natalizumabe (monoclonal antiobody) or Terifluomide
- for fatigue: Amantadine-antiviral
- for spasticity: Diazepam or Baclofen
other than MRI, what are the diagnostic criteria for MS
- two episodes or attacks of s/s
2. two diff areas of CNS involved
what kind of nerves does the tetanus toxin travel?
along motor nerves
tetanus toxin interferes with? results?
release of GABA
results: motor nerve hyperactivity and severe muscle spasms
incubation pd for tetanus toxin
3-21 days
MC presenting s/s of tetanus
Trismus–lockjaw
puncture wounds most susceptible to?
tetanus
s/s of tetanus
lock jaw
local muscle spasms
neck or jaw stiffness
dysphagia
spasm of facial muscles–CONTORTED SMILE
PAINFUL muscle spasms and rigidity progress to involve both axial and limb musculature
—-can cause apneic episodes and hyperextended posturing (opisthotonos)
contorted smile or spasm of facial muscles
tetanus
LT complications of tetanus
epneic episdoes
layngospasm and autonomic dysfunction
hyperextended posturing
TX for tetanus
hospitalize–need monitoring for resp/circulatory function
Neutralize toxin–tetanus immunoglobulin
Metronidazole for 7-10 days
diazepam to tx painful muscle spasms
Prognosis of tetanus
fatality rate 10-60%
of PTs who recover–95% have no long-term sequelae
Prevention for tetanus
Tdap
DtaP schedule
- how many doses in total?
- schedule?
FIVE DOSES IN TOTAL
2 MO 4 MO 6MO 15-18MO 4-6 YO
tDap booster given when? (4)
- 11-12 YO get a booster….afterwards it is every 10 years
- pregnant
- after major injury IF last booster was 5 yrs ago or longer
what are adults given who never had tetanus vaccine before? scheduling??
Tetanus immune globulin 250U AND initiation of tetanus toxoid vaccine:
- second dose b/w wk 4-8
- third dose given 6-12 MO after second
tetanus immune globulin given to who?
PT with contaminated wound and NO vacc hx
MS is demylelination of nerves in_____
GBS is demyelination in______
MS–CNS
GBS—PNS
desc the weakness manifestatios seen with GBS
symmetric
ascending
acquired autoimmune demyleinating polyradiculopathy of the PNS?
GBS
patho for GBS
autoantibody attacks myelin sheath of PNS AFTER AN INFECTION
Ascending paralysis begins where?
in the distal limbs
etiology for GBS
INCREASED INCIDENCE POST INFECTIONS:
- *****Campylobacter jejuni (MC)
- other GI infectinons
- Resp infections
- CMV
- epstein-barr virus
- HIV
- Mycoplasma infections
- Immunizations (BOARDS LIKE THIS ONE)**
- postsurgical
CM for GBS
often stars with symmetrical ascending weakness and sensory changes (paresthesias, pain)
**starts in distal lower extrems first
- can develop weakness of resp muscles and bulbar muscles
- dysphagia
NO CNS S/S SINCE THIS IS PNS!!!!!!
*so no bowel or bladder incontinence
what LT s/s can occur with GBS
autonomic dysfunctions can lead to death via impaired respirations via dia paralysis or aspiration pneumonia bc of aphagia
PE findings for GBS
LMN
- decreased tendon reflexes
- flaccid paralysis
- weakness
Sensory deficits
CN palsies—CN VII
Autonomic dysfunction:
- tachycardia
- arrhythmias
- HTN or hypot
- breathing problems
how do we diagnose GBS
Electrophysiologic (nerve conduction) studies
***LP: HIGH protein with normal WBC
CSF results: HIGH protein with normal WBC?
GBS
TX for GBS
First line: Plasmaphoresis or IV immune globulins (IVIG)
- prepare for mechanical ventilation
- NO STEROIDS***
What is contraindicated in tx of GBS?
steroids
prognosis for GBS
most recover within 1 year
patho for mysasthenia gravis
BLOCKADE to NM transmission:
autoantibodies attack nicotinic ACH rec–>fluctuating weakness–easy fatiguability of vol muscles
MC age and gender population for Myasthenia gravis?
YOUNG women <40 ***
older men >50 but less common
strong associationg with______ in Myasthenia gravis
abnormal THYMUS gland–75%
CM for myasthenia gravis
- generalized weakness: WORSENED WITH REPEATED MUSCLE USE….activity cannot be maintained
- Ocular weakness: diplopia & ptosis (pupils spared)
Hallmark complaint of Myasthenia gravis?
fatiguability
- worsens during the day or after PDs of prolonged use
- improved with rest
- BOARDS LOVE: weakness in everyday activities like brushing hair**
pathway of weakness for Myasthena gravis?
proximal to distal weakness:
- eyes: ptosis usually FIRST
- face: weak chewing
- limbs: easily fatigued with movement exercise
Myasthenia crisis
resp muscle weakness leds to resp failure
MC first presenting s/s of Myasthenia gravis?
diplopia and ptosis
*****ocular weakness
Diagnostic testing for Myasthenia gravis
ACH receptor antibodies**–initial test of choice
Electrophysiology testing–most accurate test
Edrophonium (Tensilon) test: when drug given, obvious improvement in muscle strength–lasts for 5 mins
ice pack test=place on eyelids for ten mins.. improves s/s
CXR, CT or MRI–done in all PT to detect thymus gland abnormalities
gold standard to diagnose MG?
Electrophysiology testing
best initial test for diagnose of MG? (OUTPT)
ACH receptor antibodies
Best initial test for diagnose of MG (emergent setting)
Edrophonium/Tensilon test
TX for severe or crisis of MG?
Plasmaphoresis or IVIG
Long term tx for MG
FIRST LINE: acetylcholinesterase inhibitors (Pyridostigmine or Neostigmine)
2nd LINE: corticos
- thymectomy–even if thymus is NORMAL—-good to do when medication doesnt work
- avoid meds that exacerbate MG
what medications are known to exacerbate MG?
Fluoroquinolones
Aminoglycosides
BBs
tremor is enhanced by? Disappears when?
- emotional stress
- disappears during stress
define static or rest tremor
EX
tremor occurs when limb/muscle is at rest
EX: parkinson tremor
Define postural tremor
EX
how to see this tremor?
tremor when skel muscle is sustained in a posture—may continue during movement but DOES NOT INCREASE with movement
*to see this tremor, ask the PT to hold out arms and hold the position
EX: essential tremor, physiologic tremor
Define intention or kinetic tremor
EX
-how to see this tremor?
no tremor at rest
but tremor starts during movement
EX: MS, chronic ETOH, cerebellar disease
**have PT do rapid finger to nose movements
tremor seen in ms?
intention or kinetic tremor
essential tremor is what kind of tremor
intentional postural tremor
MC kind of postural tremor
essential
up to _____% of essential tremor cases are familial
50%
list some activies affected by essential tremor
- eating/drinking
- writing and drawing
- getting dressed
- shaving
- tying shoes
- **when performing activities
Parts of the body an essential tremor affects
one or both hands head voice or some combo of these **legs usually spared
PE for essential tremor
finger to nose testing–tremor will increase at the end
***NO TREMOR AT REST
DX for essential tremor
clinical
- r/o other causes
- fam hx
TX for essential tremor
1st 2nd 2rd line agents
1st: Propranolol–severe cases or situational (stress)
2nd: Primidone (anticonvulsant) if propranolol not helpful
3rd: Benzo: Alprazolam
ETOH!!! can provide transient relief
what makes essential tremor worse?
stress anxiety caffeine stimulants emotional stress *intentional movement
sudden, recurrent, quick, coordinated abnormal movements that can usually be imitated w/o difficulty
Tics
can tics be surpressed voluntarily?
yes. .but for short pds of time
* doing so may cause anxiety
what worsens tics
what makes it better
Worsen with:
-stress
diminish during
- voluntary acitivity or menal concentration
- sleep
idiopathic movement disorder characterized by vocal tics, motor tics, and OCD
Tourette Disorder
what is the leading cause of acute AMS
bac meningitis
idiopathic disease due to loss of dopaminergic neurons in substania nigra
Parkinson disease
loss of dopaminergic neurons in Parkinson disease leads to failure of?
ACH inhibition in basal ganlgia
*affects dopamines ability to initiate movement
ACH is what type of NT?
Dopamine is what type of NT?
ACH=excitatory
Dopamine=inhibitory
common age of onset for parkinson
45-65YO
Parkinson triad
- resting tremor (pill rolling)
- bradykinesia–slow movements
- muscle rigidity (cogwheel rigidity)
ALL resting tremors are ____disease until proven otherwise
PARKINSON
what is the second most common neurodegenerative disease?
what is the first
FIRST: dementia
SECOND: PD
PD is characterized by?
tremor
hypokinesia
rigidity–increased resistance to passive movement (cogwheel..flexed posture)
abnormal gait and posture
what is often the first s/s of Parkinson?
resting/pill rolling tremor
bradykinesia
slowness of VOLUNTARY movement
AND
decreased autonomic movement (lack of swinging arms when walking and a shuffling gait)
is there muscle weakness and hyper/hypo tendon reflexes in PD?
NO
- no weakness
- tendon reflexes normal
what is a later finding in about 50% of PD cases?
dementia
what improves the pill rolling tremor
initiation of voluntary movement
intentional movememnt
sleep
pill rolling/resting tremor: asymmetric or symmetric?
begins asymmetric… usually one limb or one side of body… and then as diseases progresses will become generalized
explain facial involvement in PD
"fixed" facial expression immobile face -widended palpebral fissure "masked facies" decreased blinking *seborrhea is a common skin condition
Myerson’s sign
tapping the bridge of nose repetitively causes sustained blink
tapping the bridge of nose repetitively causes sustained blink
seen with?
Myerson;s sign
PD
DX for PD
clinical
- no lab tests or physiologic testing for dx
- can R/O structural abnormalities with MRI
POST-MORTEM HISTOLOGY: only time we can officially dx
- Lewy bodies
- loss of pigment cels in susbtantia nigra
TX for PD
- most effective
- what is 1st line
- drug to use if tremor only s/s
- Drug used in early cases wth mild s/s
- Levodopa-carbidopa–but long term use wears off after 10 years.. why we wait to start this drug until older >65 YO
- Dopamine agonist–Bromocriptine (>65YO)
- Anticholinergics–Trihexyphenidyl (does not help w/ bradykinesia)
- Amantadine–increases dopamine
what happens if you pull the shoulders back of a PD PT?
they will fall or take step backwards
*bc they have postural instability
typical age of onset for tourette?
childhood (4-6)
MC gender for tourette?
M>W
MC intitial presenting symp for Tourette?
motor tic–involving head, face or neck
- blinnking
- shrugging
- head thrusting
- sniffling
DX criteria for tourette
Multiple motor or 1+ vocal tics for >1 year
Onset prior to age 18
TX for tourette?
-first line
Most dont need pharmacotherpay
*habit reversal therapy is FIRST LINE aka CBT
Pharmaco:
- Dopamine blocking agents: Tetrabenzaine
- Alpha 2 adrenergics: Clonidine (sedating)
- Clonazepam for adjunct tx
TX for refractory cases of tourette?
deep brain stimulation
