Neuro Last Test Flashcards
Define vertigo
A sense of rotational motion. Indicates a dysfunction with the vestibular pathways
Define disequilibrium
Being “unsteady”
About to fall
And is often associated with some type of abnormal gait
Define light headed es
The sensation that one is about to faint
Define presyncope
Presyncope: used to describe a transient cerebral hypo perfusion. Often a prodrome to a true syncopal event
What is benign disequilibrium of aging
Multiple-sensory-defect dizziness :
Elderly when walking
Define syncope
A transient decrease in blood flow to the brain, resulting in a loss of consciousness.
Characterized by sudden loss of consciousness, and postural collapse, with spontaneous recovery.
Will be experienced by at 30% of the adult populations and accounts for about 3% of ER visits
So…..anything that decreases blood flow and decreases O2 to the brain can cause syncope
What are the 3 types of Syncope
Neurally mediated
Orthostatic HOTN
Cardiac Syncope
What are the two types of Neurally mediated syncope
Vasovagal and reflex
Define Vasovagal Mediated Syncope
Provoked: fear, pain, anxiety, intense emotion, sight of blood, unpleasant sights and odors, orthostatic stress
Sympathetic withdrawal – vasodilation
Increased parasympathetic activity – bradycardia
They account for nearly 1/2 of all syncopal episodes
Often present with a prodrome – seconds to minutes before\
Diaphoresis, pallor, nausea, yawning
Rare in the supine pt
Refine reflex mediated syncope
specific localized stimuli that provoke the reflex vasodilation and bradycardia that leads to syncope
A pt presents with a LOC, first had TachyHR and now is Brady,
Has an ashen-grey color
(pallor in the conjunctiva)
Has a threads pulse and may have clonic jerks of the face and hands
They quickly regain consciousness with a brief ep of confusion
What type of syncope event is this
Vasovagal
A solider just passed out in formation from a Vasovagal syncopal event
What is the Tx
Place the patient in the supine position with feet slightly elevated
Feel improved pulse
Consciousness should gradually return
Treat underlying causes
Define Carotid Sinus Hypersensitivity
Caused by increased pressure on carotid sinus baroreceptors
Is a reflex syncope
Typically occurs after shaving, wearing a tight collar or simply turning the head to one side
Usually in men > 50 yo
S/S: Sinur arrest, AV blocks, vasodilation, mixed response
Cause; Afferent nerve fibers activate the efferent sympathetic nerve fibers in the heart and blood vessels
Define Situational syncope
A type of reflex syncope
Cause by an abnormal autonomic control
May involve a:
- Cardio-inhibitory response
- Vasodepressor response
- or both
Can be from cough, deglutition, micturition, defecation
Define glossopharngeal neuralgia
Likely involves activation of afferent impulses in the glossopharyngeal nerve that terminate in the nucleus solitarius of the medulla
Less likely to have a benign origin: vascular compression, MS, or tumors.
Many cases are idiopathic.
More prevalent in elderly
Symptoms – bradycardia, hypotension, fainting, and asystole
Pain very similar to Trigeminal Neuralgia
Sharp, repetitive pain precipitated by: Swallowing Chewing Talking Yawning
What is the Tx approach to Glossopharyngeal Neuralgia
Start with:
-Carbamazepine (anti-epileptic drug)
If meds fail consider surgical intervention
Microvascular decompression if vascular compression is evident
Rhizotomy of Glossopharyngeal/Vagal fibers
Define Ortho HOTN
systolic blood pressure drop of at least 20 mmHg or diastolic blood pressure of at least 10 mmHg within 3 min of standing
Common causes:
Polypharm
Diabetes, Dehydration, being weak
What is the Tx approach to Ortho HOTN
1st: remove causes
(meds if applicable)
2: mitigate risk
3: if unable to still control
Consider: with fludrocortisone acetate and vasoconstricting agents (midodrine, L-dihydroxyphenylserine, and pseudoephedrine )
A Pt presents with syncope without any prodrome, asso with exertion or post exertion
What type of syncope is high on the DDx
Cardiac Syncope
What is the likely cause of syncope when it occurs when the pt is lying down
CV
A pt presents with Impulsion, oscillopsia, N/V, and gait ataxia
Think
Vertigo
What is the DIx-Hallpike maneuvaer
This test is performed by rapidly moving the patient from a sitting position to the supine position with the head turned 45° to the right. After waiting approximately 20-30 seconds, the patient is returned to the sitting position. If no nystagmus is observed, the procedure is then repeated on the left side.
Test for Vertigo causes
This is performed initially for the posterior semicircular canals.
What are saccades and pursuits of the eye
Saccades – fast eye movements
Pursuit – slow eye movements
A pt presents with long episodes of iunchanging dizziness
Not affected by head position or movement
+nystagmus
With hyper reflexia, ataxia, and dysarthria
Is this central or peripheral vertigo
Central
A pt presents with intense short lived epidsodes of dizziness, typically effected by head position, with HORIZONTAL nystagmus without vertical nystagmus, with inner ear sxs, and hearing abNML
What kind of vertigo is this?
Peripheral or central ?
Peripheral
Describe vestibular neuronitis
Usually a single attack, with paraoxysmal vertigo
Has preserved auditory function
Lasts several days to weeks
May be related to viral illness
+nystagmus
What is the Tx for Vestibular neuronitis
Most Pts recover spontaneously
Glucocorticoids may improve outcome
—if given in first 3 days
Vestibular Suppressant meds
—Diazepam (benzodiazepine) 5 to 10 mg every twelve hours
—Meclizine (antihistamine) 25 to 50 mg every eight hours
Vestibular therapy if not completely resolved over time
No proven benefit to Antivirals !
Describe labyrinthitis
Same S/s as vestibular neuronitis WITH hearing loss
Cause unknown
Hearing loss can be perm.
What is the Tx approach to Labrythitis
TX:
ABX
-If febrile
-Signs of infection
Vestibular suppressants in acute phase
- Diazepam
- Meclizine
What is the major diff between vestibular neuronitis and labrynthitis
Hearing loss is not preserved in labrythitis
Treatment for Vestibular involves steroid (glucocorticoids)
And Labrythinitis does not
Both treatments involve Diazepam and/ or meclizine
Labrythitis can get ABX if fever
What is the MC cause of vertigo following a concussion
Labyrinthine Concussion- Traumatic Vertigo
Sx usually diminish after several days
If associated with basilar skull fracture:
- Severe vertigo
- Lasting several days to weeks
- Deafness in affected ear
Chronic Post-traumatic may result from cupulolithiasis
- This causes excessive cupular deflection with head movement
- Causing episodic positioning vertigo
A pt presents with labrynthitis s/s following a head concussion
What is the tx appraoch
Supportive care
Vestibular suppressants
-Diazepam (benzodiazepine)
-Meclizine (antihistamine)
Vestibular therapy
What is the Triad of Menieres Dz
TRIAD
- Unilateral deafness
- Episodic/paroxysmal vertigo
- Unilateral Low freq. tinnitus
A pt presents with vertigo lasting from minutes to days, unilateral deafness, and unilateral low freq tinnitus
What is the likely pathology
This is the triad of Menieres Dz
Pathology: thought to be 2ndary to excess fluid in the inner ear
For a pt with fluid found in the middle ear and the triad of Menieres dz what must you submit the pt for
DX: Audiometry for all patients!
Consider Vestibular testing and MRI.
- Sometimes can only be made for certain on pathologic examination of a gross-section of the cochlea (biopsy)
What is the Tx approach to Menieres Dz
Change Diet: avoid high salt, caffeine, alcohol, nicotine, and MSG
Reduce Stress,
Diuretics to remove excess fluid
(HCTz/ Triamterine)
N/V: Meclizine, scopolamine, and diazepam
+/- Hearing aids
Last stage: SRGRY or middle ear injection with ABX (genta)
What causes a perilymphatic fistula
Caused by
Leakage of perilymphatic fluid from the inner ear that drips into the tympanic cavity
Most cases are caused by:
Physical injury:
-Blunt head trauma or a Hand slap to the ear
Extreme barotrauma: Air flight or Scuba diving
Vigorous Valsalva maneuvers: Weight lifting or Cough/Sneeze
After middle ear surgery
What is the Tx for perilymphatic fistula
Conservative Management: bed rest, head elevation, and avoidance of straining
Failure to resolve after several weeks of conservative therapy is an indication to consider a surgical patch of the oval or round window
A pt presents with benign paroxysmal postional vertigo
What are the common S.s
Brief, sudden episodes of severe vertigo
Typically w/ nausea & vomiting
Occur with change in head position/posture
What is the management of BPPV (vertigo)
Meclizine q 4-6 hrs
Valium 5mg TID
+/- scopalamine patch
+ Epley maneuver
Define acoustic neuroma
Benign tumor arising from the sheath of CN VIII in the internal auditory canal
AKA, Acoustic schwannoma
Arises from the Schwann cells
(Dip in the 4000 MgHrtz)
MC to CN VIII
Can be in CNV or VII
Presents with insidious onset hearing loss; also tinnitus, HA, vertigo, facial weakness
Unilateral Sensorineural hearing loss on exam
What is the presentation, Dx and Tx of Acoustic Neuroma
Presentation May be asymptomatic Loss associated with the affected CN Hearing loss Vestibular symptoms Facial paresthesia Pain
Imaging: MRI with contrast
TX
If symptomatic, non-compressible, and < 3 cm
Stereotactic radio surgery – gamma knife
What is the best test to find a Acoustic Neuroma
MRI with contrast
Define Vestibular migraine
Episodic vertigo
Temporarily related to HA
Lasts from minutes to hours
Have have a positioning component
Disequilibrium may last days to weeks
Define central disorders that cause vertigo
Central vertigo is due to a disease originating in the CNS
Lesions within the brain itself
—Cerebellum
—Pons
Disorders present with ataxia, vertigo and often with nystagmus
(Central S/s)
Symptoms present slowly over several months
Little or no change in symptoms with head movement
A tumor in the cerebellum would present with
Incoordination
A tumor that is in the basal ganglia would present with
Impaired postural reflexes
Basal ganglia: are the caudate nucleus, putamen, and globus pallidus in the cerebrum
A tumor that is in the sensory tracts would present with
ABNML proprioception
What are the causes of chronic central vertigo
MS
ETOH induced
Hypothyroid
Congenital
What are the 5 common causes of central vertigo
- Vertebrobasilar Ischemia/Insufficiency
- Vertebrobasilar TIA or Stroke
- Tumors
- Multiple Sclerosis (demyelination) (p
- Neurodegenerative conditions that include the vestibulocerebellum
A pt presents with vertigo plus Diplopia
Dysarthria
Ataxia
Numbness
Think:?
Central Vertigo cause
Vertebrobasilar Ischemia/Insufficiency
Order an MRI (ischemic infarct)
and send to higher level of care
Describe a TIA or Stroke
Caused by infarcts into the medial branch of the PICA
Sudden onset
Difficulty maintains posture
Infarct or hemmorghe
Order a CT/ MRI
How do you manage a TIA or Stroke
Workup R/O Anemia Pregnancy Glucose derangement
MRI preferred modality to detect: Infarction Hemorrhage Tumor White matter lesions of MS
Intra-arterial angiography to Dx:
Occlusions
—This getting supplanted by CT angiography, noninvasive
MR angiography, and Doppler US
Central causes: Referral to higher care
Wernicke’s = Thiamine replacement
MS flare – Prednisone burst
Avoidance of offending agents.
What do you treat wernickes stroke with
Thiamine replacement
What do you treat a MS flare with
Presdnisone
What are the drugs that can cause central vertigo
Gentamycin
Salicylates
Quinine
Cis-platinum
Define SZR
Seizure: transient occurrence of signs or symptoms due to abnormal excessive or synchronous neuronal activity in the brain.
Aura: brief symptoms that may precede the onset of some seizures
Epilepsy: group of disorders characterized by recurrent seizures
What are the three Etiologies of SZR
Primary CNS dysfunction
Underlying systemic disease
Drug induced
What are the 5 physiological conditions that can lead to SZR
HOgl (if glucose less than 30)
HONa+ ( is less than 120)
Hyperosmolar (Non Keto Hypergl)
HOCa2+ (less than 9.2, with or without tetany)
Uremia (greater than 19, or rapid decline in KD function)
What is the approach to evaluating a SZR
- Real or not?
- Clues to predisposition
(Head truama, Stroke, tumor) - Precipitating fxs
(Sleep deprivation, drugs, alcohol) - Infection? Systemic illness?
- Truama?
- Complete Neuro Exam
- Order Labs, glucose, calcium, BMP, ESR, BUN, Cr, LFTS
- Initial SZR imaging is a MUST!
(MRI is superior to CT)
(In ER CT non con is sometimes best)
What does a FTA-ABS lab test
Syphillis
Focal vs gen SZRs
Focal Seizures:
- Originate within networks limited to one brain region
- Previously called partial seizures
Generalized Seizures:
- arise within and rapidly engage networks distributed across both cerebral hemispheres
Describe a focal SZR with INTACT awareness
Motor manifestations
Tonic: muscles stiffen
Myoclonic: extremely brief (<1sec) muscle contraction
Clonic: rhythmical muscle contractions
Two Named Versions
-Jacksonian March
seizure activity over a progressively larger region of motor cortex
-Todd’s Paralysis
localized paresis for minutes to hours in the involved region following the seizure
What is Jacksonian March
Jacksonian March:
seizure activity over a progressively larger region of motor cortex
What is Todds Paralysis
Todd’s Paralysis:
localized paresis for minutes to hours in the involved region following the seizure
Describe Focal SZR with IMPAIRED awareness
Transient impairment
Unable to maintain nl contact w/ environment
Unable to respond appropriately
Impaired recollection of the ictal phase -Aura -Automatisms —involuntary, automatic behaviors that have a wide range of manifestations —chewing, lip smacking, swallowing
Describe an absent SZR
Sudden, brief lapses of consciousness
Lasts for seconds
No postictal concussion
No loss of postural control
Onset childhood/early adolescence
100s X per day
“Daydreaming”, Decline in school performance
Electro physiologic hallmark (typical)
Generalized, symmetric, 3-Hz spike-and-slow-wave discharges that begins & ends suddenly, superimposed on a nl EEG background
What is the most common SZR type in a metabolic derangement
Gen Tonic Clonic SZR
What are the three phases of a GEn Ton Clon SZR
Tonic phase to Clonic Phase to Postictal phase
What is the Tonic phase of a Gen Ton Clon SZR
Tonic Phase: extension of body
Lasts about 10-20 seconds
May have apnea
Tongue biting
EEG: progressive increase in generalized low-voltage fast activity, followed by generalized high-amplitude, polyspike discharges
What is the clonic phase of a Gen Ton Clon SZR
Clonic Phase: alternating muscle contraction and relaxation
Lasts no more than 1 minute
EEG: high-amplitude activity is typically interrupted by slow waves to create a spike-and-slow-wave pattern
Describe the postictal phase of a Gen Ton Clon Phase
Postictal Phase:
Unresponsiveness & muscular flaccidity
Excessive salivation
Bladder or bowel incontinence may occur at this point
Postictal confusion for minutes to hours
EEG: diffuse suppression of all cerebral activity, then slowing that gradually recovers as the patient awakens
Describe an Atonic SZR
Sudden loss of postural tone
Lasts 1-2 seconds
Consciousness is briefly impaired
Zero postictal confusion
EEG: brief, generalized spike-and-wave discharges followed immediately by diffuse slow waves that correlate with the loss of muscle tone
Describe a Myoclonic SZR
Cause sudden jerking in the muscles
May involve one part of the body or entire body
Normal common form (physiologic form) is sudden jerking movement and when falling asleep
Pathologic form is associated with metabolic disorders, degenerative CNS disease or anoxic brain injury
EEG: bilaterally synchronous spike-and-slow-wave discharges
What is the main type of SZR in epilepsy
Gen Clon Ton SZR
What is the pt education for Epilepsy
No heavy machinery or at heights,
No swimming alone
Patients with epilepsy are generally undereducated and underemployed for their level of function
Issue of driving must be addressed: most states require a 3-18 month seizure-free period before pt may resume driving
Medical Providers are responsible to
warn patients of danger to themselves or others when driving with uncontrolled seizures
What is the gen appraoch to SZR treatment (epilepsy)
Underlying cause!
Avoid triggers
Alcohol or stress, sleep deprivation
Rx is the mainstay
Always watch for new rash/ Steven Johnsons syndrome!
What is are the Rx options for Absence SZRs
Valproic acid
Ethosuximide (Zarontin)
—May cause bone marrow suppression
All anticonvulsants have what side effects
All anticonvulsants may lead to hematologic or hepatic toxicity
CBC and LFTs at 2 weeks, 1 month, 3 months, 6 months, and every 6 months
What are the Rx options for Focal SZRs
1st line
Lamotrigine (Lamictal)
SE/AR: Stevens—Johnson Syndrome
Carbamazepine (Tegretol)
SE/AR: leukopenia, aplastic anemia, heptotoxic
Oxcarbazepine (Trileptal)
SE/AE: less risk of the above
Phenytoin (Dilantin)
Awful Cosmetic SE/AR: Gingival
Hypertrophy (AVOID IN YOUNG PTS)
Levetiracetam (Keppra)
No known drug-to-drug interactions, great for elderly !!
What are the Rx options for Gen Clon Ton SZRs
First Line
—Lamotrigine (Lamictal)
SE/AR: Stevens—Johnson Syndrome
—Valproic acid
Laboratory testing is required to monitor toxicity because valproic acid can rarely cause reversible bone marrow suppression and hepatotoxicity.
—Levetiracetam
No known drug-to-drug interactions, great for elderly
When can you step down Tx for SZRs
Seizure free x 1-5 years (typically 2)
Single Seizure type
NML Neuro Exam
No FMHx of Epilepsy
NML EEG
Define Status Epilepticus
Prolonged seizure activity lasting 5 minutes or more
Continuous seizure
Discrete, recurring seizures with unconsciousness during ictal period.
Is a medical emergency: -Cardiorespiratory dysfunction, hyperthermia, and metabolic derangements can develop
Mortality rate for adults with first episode of status epilepticus: 20%.
What are the common causes of Status epileticus
Anticonvulsant withdrawal/noncompliance
Metabolic disturbances
Hypoglycemia
Drug toxicity
CNS infection
CNS tumors
Refractory epilepsy
Head trauma
What are the Rx options to treat status epilepticus
First Line
Lorazepam, or Midazolam, or Diazepam
Followed by
Phenytoin or Fosphenytoin
If fails, then general anesthesia w/ ventilatory support
If a pt has recurrent SZRs despite RX tx,
What is the approach ?
Determine serum level of drug
MRI to rule out structural lesion
Evaluate lifestyle factors that may be contributing
Change to a second drug
Referral to neurologist if seizures are not controlled within three months
Treating refractory seizures: surgical excision, vagus nerve stimulation
If first drug achieved partial control, consider adding a second drug:
-referral
Best addressed with neurology consultation
What are the 3 most important pieces of HPI
Baseline Function
Time of Onset
—slow
—step wise
—acute?
Current meds
A pt presents (child) with sig high fever
What derm condition is indicative of meningitides
Skin rash of the lower extremities
What is the ABN number of a mini mental status exam
Less than 24 requires addition testing
What are the essential elements of a mental status exam
Comprehension Repetition Fluency Naming Reading Writing Speech
What are the 5 types of aphasia
Global!
Conduction!
Transcoritcal motor
Transcoritcal sensory
Subcortical
What is global aphasia
Fluency is impaired, repetition is impaired, comprehension is impaired, may have a associated severe Right hemiparesis, caused by a large lesion in the Left hemisphere
What is conduction aphasia
Fluency is preserved, comprehension is preserved, but repetition is severely impaired . Naming and writing are also impaired.
Describe working memory
<30 seconds 7 bits of information (+/- 2) Vulnerable to distraction Anatomically related to the RAS, Prefrontal cortex, and Parietal lobe. Tested with “repeat after me”
What is episodic memory
Lasts for minutes to many months or even years
Binds information about “What,” “Where,” and “When”
“Lay down” significant memories throughout the day which allows them to move through life connected to previous experiences.
Anatomically related to Hippocampus, Dorsomedial nucleus of the thalamus.
This is affected in thiamine deficiency.
Tested with word recall @ 3-5 min, or by asking of trivial events of the day – “What did you have for breakfast?”
Describe lasting memory
Lifelong – related to new protein synthesis and creation of new synapses
Lt. Anterior temporal lobe
And
Frontal lobe
What is the term Mental activities involved in planning, initiating, and regulating behavior.
Executive function
Define delirium
Typically acute in onset
Responds to at least some stimuli appropriately
Can appear sleepy, disoriented, and inattentive
Level of consciousness may be impaired
Any age
Typically reversible
define dementia
Typically chronic in onset with worsening over time
Usually appear “normal” but confused
Normal level of consciousness
Impairment in the content of consciousness
Typically more elderly (but not always!)
Irreversible
What is the hallmark description of delirium
Hallmark description is waxing and waning levels of consciousness.
What happens to GABA when a long term drinker stops drinking?
Decrease GABA
A pt presents with anxiety, tachyHR, and agitation
PHx is +ETOH abuse
+delirium tremens
What is the D/o and Tx?
Withdrawal;
Treat with Benzo
upcoming Tx options Gabapentin
What is the MC found vit deficiency in ETOH abuse
Thiamine deficiency Most Commonly in the chronic alcoholics
Leading to wernickes encephalopathy
Characteristic clinical triad of: -Ophthalmoplegia/ Nystagmus
- Gait Ataxia
- Global Confusion
Requires prompt Thiamine replacement
A pt presents with Ophthalmoplegia/ Nystagmus, Gait Ataxia, and Global Confusion
What is this a classic triad of
Wernickes encephalopathy from Thiamine deficiency
all patients with undiagnosed altered mental status, oculomotor disorders, or ataxia should receive …
Parenteral Thiamine
What is Korsakoffs psychosis
Deficits in learning and memory may follow wernickes encephalopathy (Korsakoff’s psychosis) characterized by gaps in memory, confabulation, and disordered temporal sequencing.
What is the main risk factor for dementia
Age, followed bu FMHx and Risease Risk
A fall of 1.5 standard deviations below normal on standardize memory test is Dx of
Mild cognitive impairment
Does Dementia impact function?
No
What are the risk factors for Cognitive impairment leading to Dementia
Memory deficit >1.5 SD from the norm
Presence of Apolipoprotein ε4 allele
Small hippocampal volume & low CSF
FHx of dementia
What are the 3 steps of Alzheimer’s disease (typical)
1st memory impairment
2nd Language/visuospatial deficits
3rd Executive dysfunction
What are the risk fx for Alzheimer’s
Risk Factors for AD:
Age > 70
(+) FMHx of AD
Diabetes increase risk of AD by 3x
The major genetic risk:
ε4 allele of the apolipoprotein E (ApoE) gene
Define Alzheimer’s pathology
neuritic plaques of AB42 amyloid and neurofibrillay tangles
What is the diff of Cognitive Impairment and Alzheimer’s
AD impaires function and MCI retains function
What are the Tx approaches to Alzheimer’s
Behavior MGMT
Rx: Drugs: Cholinesterase Inhibitors -Donepezil 10mg daily target dose -Rivastigmine 6mg twice daily -Galantamine ER 24mg daily
N-Methyl-D-aspartate (NMDA) receptor antagonist
-Memantine 10mg twice daily
What are the findings in End Stage Alzheimer’s
Physically: Rigid, mute, incontinent, bedridden
Hyperactive DTRs, myoclonic jerks
Death
Most common aspiration
Malnutrition, 2ndary infxn, PE, CAD
Typical duration of symptomatic AD is 8-10 years
Define Vascular Cognitive Impairment/ vascular dementia
strongest Rsk fx AGE (70)
Dementia arising from a vascular insult/ cerebrovascular dz
(Infarcts)
Describe Frontotemporl Dementia
Most common behavioral variant
Has three variants ;
behavioral
Primary Progressive Semantic
No fluent/ Agrammatic variant
Group of Clinical Syndromes
Frontotemporal lobe degeneration
Presents in 5th to 7th decade of life
EARLY behavior decline
(Alzheimer’s is Late behavioral decline)
What is the gross hallmark of FTD pathology
Atrophy of frontal and/or temporal cortex on MRI
Microscopically:
misfolded tau protein
Are the any Txs for FTD?
NO, sadly sadly NO
Define Dementia with Lewy Bodies
Dementia syndrome characterized by
- Visual hallucinations
- Parkinsonism
- Fluctuating alertness
- Sleep behavior disorder
Delusions common
Microscopically
-Lewy bodies throughout the brain
What is the Tx approach to Dementia with Lewy Bodies
Cholinesterase Inhibitors
Excercise and Antidepressants
What are the three most common reversible causes of Dementia
Depression
hydrocephalus
ETOH dependence
Define psuedo dementia
Depression is most commonly mistaken for dementia.
Both show mental slowness, apathy, self-neglect, irritability, difficulty with memory, etc…
All patients with suspected dementia must be screened for depression and anxiety.
Define Dementia vs Depression
Dementia: Pt unaware of deficits No c/o memory loss Few sedative symptoms Worse at night AbNML Neuro Exam AbNML Labs possible
Depression:
They are aware of deficits
With C/o memory loss
Not worse at night
What is the Tx approach to Psuedodementia
TX the depression
SSRI, SNRI
CBT
What is the classic triad of NML pressure hydrocephalus
Cognitive decline (dementia)
Urinary Incontinence or Urinary Urgency
Gait difficulty
What is the managment Tx for normal pressure hydropcephalus
Shunt
In a pt that has a thiamine deficienty and low glucose
Which should be replaced 1st
Thiamine
Define basal ganglia
Central processing center of the brain
Movements
Cognition
Emotions
learning
Define essential tremor
Goes away during sleep
And goes away with ETOH ingestion
Rhythmic oscillatory movement characterized by its relationship to voluntary motor activity
Increases with stree
Define Chorea
Dancing, flailing type tremor
Decreased grasp “milkmaid”
Often falls
Irregular speech
Irregular gait
“Dancing gait”
Define Hemiballismus
Unilateral chorea
Most often due to vascular Dz or stroke.
Tx: dopamine depleting/ blocking agents
Severe: pallidotomy
Define Athestosis
Restless
Slow, sinuous involuntary
Can lead to dystonia
Define Dystonia
Sustained muscle contractions frequently with twistings and repetitive movements
Not present during sleep
Focal:
- Torticollis
- Blepharospasm
- Writers cramp
Generalized:
Cerebral Palsy
Acute Dstonia
Define Tardive dyskinesia
Involuntary movements of the face or tongue
After antipsychotics drugs or Reglan
Define Myoclonus
Sudden rapid twitch like muscle contractions
Can be generalizes, fovcal, multi focal
Or segmental
Define TIcs
Brief, rapid, recurrent, purposeless moments
Can be motor or phonic
Simple or complex
Tourette’s- COmplex
Coprolalia
Profanity
Echolalia
repetition of sounds
Define Parkinsonian tremor
4-6hz tremor
Most copious at rest
Increased with stress
Improves with activity
Define cerebral tremors
Result from stroke, tumor, or disease (MS)
Often with dysarthria, nystagmus, and gait problems
Define a psychogenic tremor
Functional tremor
Assoc with conversion D/o
SUDDEN ONSET
Decreased with distraction
Define orthostatic tremor
Rhythmic muscle contractions
Occurs in legs or trunk
Most notably after standing
“Unsteadyness”
Decreases with sitting, or walking
Physiologic tremor
What is the gene mutation associated with the most common tremor
Essential tremor is the most common tremor
Gene: EMT1 and 2
Acute dystonia and tx
Remove any offending agents plus diphenhydramine and baclofen
Drugs that are assoc with Dystonia RXNs
Anti psych drugs
Phenytoin
] Phenothiazines- eg. chlorpromazine (Thorazine); Fluphenzaine (Prolixin)
Haloperidol (Haldol)
Atypical antipsychotics (fewer side effects/extrapyramidal symptoms) Eg. Olanzapine (Zyprexa), Resperidone (Risperdal)
Phenothiazine anti-emetics (also act as dopamine antagonists)
eg. Promethazine (Phenergan), Prochlorperizine (Compazine)
Cocaine, LSD
Tricyclic antidepressants - eg. Amitriptyline
Lithium
Anticonvulsants: Phenytoin, Carbamazepine
Tx approach to acute dystonia Slide 30 lecture 8
4 core symptoms: An urge to move the legs with or without sensations Worsening sx’s with rest Improvement with activity Worsening in the evening or nights
What is this
RLS
Define Tourette Syndrome
Effects Boys more than girls
Chronic and life long
Multiple motor and verbal tics
assoc: OCD and ADD
Dx: prior to age 21
What is the Tx approach to Tourette’s
Ed and counseling
Haloperidol to reduce tics
Clonidine reduces tics
Also
Fluphenzaine and Botulinum Toxin A
Define Parkinsonism
Any clinical syndrome that relates to Parkinson’s Dz
4 causes: Neuroleptic Drug Exposure Cerebrovascular Dz Methyl-phenyl-tetrahydropyridine Encephalitis lethargica
Any combination or presentation of Tremor Rigidity Bradykinesia Postural instability Cognitive impairment
define Parkinson’s Dz
A complete combination of all 4: Resting tremor Cogwheel Rigidity Bradykinesia Gait impairment
What is the pathophysiology of Parkinson’s Dz
Damage to the Substantia Nigra with cell loss in basal ganglia
Dopamine exerts an inhibitory effect on release GABA
Without dopamine, GABA output increases
What are the late features of Parkinson’s Dz
Disregulation of autonomic sys
Ortho instability
Dementia
Skin greasiness, seborrhea
What are the Tx approaches to Parkinson’s Dz
Dopamine Agonist
(Pramipexole, Ropinirole)
And Dopamine replacement
Anticholinergics can reduce gritos and tremor
(Benzotropine)
Define Huntingtons
Genetic autosomal transmission
Onset 25-45
Genetic mutations causes premature cell death, resulting in atrophy in cerebral cortex and caudate
Concentrations of GABA and ACh in the basal ganglia are reduces which INCREASE dopamine
What is the treatment approach to huntingtons Dz
Treat the S.s
Haloperidol -block movements
Reserpine- can delplete dopamine
SSRI- moodiness and aggression
Benzos- help with sleep and anxiety
What is the largest S/s finding of cerebral palsy
Spasticity
Define Wilson Dz
An autosomal recessive disorder
Increased copper levels in the blood
Build up in the CNS, Cornea, and kidney
S/s: Tremor, ataxia, Dysarthria, Dyskenisia, Parkisoninsim
KAYSER FLEISHER RINGS
What are the three most predictive exam finding for acute stroke (ischemic)
Asymmetric facial paresis
Arm drift/weakness
Abnormal speech (dysarthria)
What are the major RSk factors for stroke
Primary Arterial Hypertension
A. Fib
Smoking
Medical HX
Previous TIA
1/3 will have a full stroke in 5 years
Age
What is the most common vascular pathology that causes Ischmic strokes
Atherosclerosis
Define anoxic brain injury
Decreased blood flow to the brain from Low systemic perfusion pressure
Most common cause is from: -Cardiac pump failure due to MI -Arrhythmia -Systemic hypoperfusion -Blood loss -Hypovolemia
The lack of perfusion is more generalized and affects the brain diffusely and bilaterally
Describe lacunae infarcts
Small Vessel Disease
(AKA Lacunar Infarcts)
Small (0.5-1.5 mm) arteries from…
-Distal vertebral artery
-Basilar artery
Middle cerebral artery stem
Causes -Lipohyalinosis -Atheroma formation (fatty deposits) -arteriolosclerosis
What is the most important DX test in Stroke pts
Noncontrast CT!
Ischemic stroke – looks dark - may be normal in first 24 hours
Hemorrhagic stroke – looks bright/white - should show up earlier
How do hemorragic strokes appear on CT
Noncontrast CT: acute hemorrhage appears bright on CT scan, whether in the brain itself, or outside the brain parenchyma (subarachnoid, subdural hemorrhage).
Sensitivity: 89%; specificity: 100%
What are the C/I to thombolysis in stroke Pts
Sustained BP >185/110 mmHg despite treatment
Bleeding disorder/diathesis
(plt <100,000, HCT <25%)
Recent head injury/stroke/intracerebral hemorrhage
(in the prior 3 months)
Major surgery in the past 14 days
GI bleeding in the previous 21 days
Recent Myocardial Infarction
(in the prior 3 months)
How does ischemic stroke present on CT
DARK AREAS!
White areas mean its hemmorhagic
What is the timeframe for TPA administration
Within 3 hours!
If a pt is not a candidate for tPa what should be done for their stroke?
If not candidate for Tissue Plasminogen Activator (tPA), should be given ASA, after exclusion of hemorrhage on CT.
Manage BP, vitals and complications of stroke
i.e. swelling
What is permissive hypertension in Ischemic Stroke
Permissive hypertension:
Don’t let the SBP >220,
or DBP over 120
- B1-adrenergic Beta-blocker such as esmolol
- works by relaxing blood vessels and slowing heart rate to improve blood flow and decrease blood pressure.
What are the vascular screening methods for Strokes
Carotid Doppler:
-Used in the evaluation of suspected stenosis of the intracranial internal carotid artery, middle cerebral artery, or basilar artery.
MRA
Conventional xray angiography is “gold standard” for AVM or SAH but has a 1% risk of stroke during procedure.
What are the three steps to stroke tx
Identify the stroke
Plan of action: lytics and Anticoagulant
Long term prevention
A pt presents with sudden severe HA followed by LOC,
Think DDX
Aneurysm (berry)
What is the most common medically cause of SAH
Ruptured cerebral aneurysm
What are the two common morphologies of SAH
-Saccular- (most common)
Aka Berry/ Congenital that occurs at the bifurcation of the large cerebral arteries at either the circle of Willis or at the MCA/Sylvian fissure
Or
-Fusiforme
What are the 4 hallmark S.s of SAH
headache
Syncope
Nausea
Vomiting
Subhyaloid retinal hemorrhages are a sign of…
Intracranial Hemm,..
most likely SAH
A pt presents with Severe HA, with retro orbital pain, and a stif neck
Think
SAH
A pt presents with 3rd cranial nerve palsy, with diminished light reflex and pupillary dilation
Think what bleed in the brain
PCA! In the circle of Willis
What are the imaging of choice for SAH
NOn Con CT
If pos then send for cerebral angiogram
If neg, evaluate lumbar puncture
Positve RBCs?
What is the gold standard imaging for SAH
Cerebral angiography
What is the tx approach to SAH
Absolute bed rest
EHOB 15-20 degrees
Mild Sedation
Stool softeners
Maintain platelet function
Treat Hyponatremia
CCB to reduce vasospasms
(Nimodipine)
Cerebral artery angioplasty
Anticonvulsants to reduce SZR
What are the 4 major complications of SAH
Cerebral ischemia: from vasospasm
Acute hydrocephalus: from clot
Bleeding: from the rupture
Increased risk of future normal chronic hydrocephalus
What two groups have increased risk of Intracerebral Hemorrhage
Asians and African Americans
What is the classic location of intracerebral hemm.
Basal ganglia due to HTN
Common in African Americans
What is the approach to BP control in HEMORRHAGIC stroke
Intracerebral hemorrhage:
Presents w/ acute ICH SBP
150 – 220 then lower to 140mmHg
> 220mmHg then lower
140 -160mmHg
Subarachnoid hemorrhage
-Keep SBP lower than 160 mmHg
Monitor for signs of cerebral hypoperfusion
Stop all antiplatelet/anticoag drugs or reverse
What is an AVM
Arteriole-Venous Malformations
Congenital Art. Venous connections w/o a capillary bed in-between
High flow of blood
Not completely normal blood vessels
What is the most common brain vascular malformation
DVM!
These are composed of anomalous veins
These are morphologically different from brain parenchyma
These have one or more central draining vein that are Conspicuous
May be dilated into a varix or varices
What is a Cavernous Angiomas
These are a relatively compact mass of sinusoidal vessels
They are packed close together
They have no intervening brain parenchyma
They are well encapsulated
Form within deep hemisphere white matter and brainstem without normal intervening neural structures
What is telangiectasia’s
True capillary malformations that often form extensive vascular networks through an otherwise normal brain.
Pons and deep cerebral white matter are typical locations.
If bleeding does occur, it rarely produces a mass effect or significant symptoms.
No treatment options exist.
What is the treatment for vascular malformations
All are tx with
- Medical therapy to reduce seizures
- Surgery to prevent rebleeding
- Interventional obliteration
- Radiotherapy
Tx depends on presentation
What is the most common MOI in younger individuals
TBI from MVA
What is the most common MOI in older adults
Falls
Define TBI
alteration in brain function caused by an external force and characterized by the following:
- Any loss or decreased consciousness
- Any loss of memory for events immediately before (retrograde) or after (posttraumatic) the injury
- Neuro deficits and/or alternation in mental state at time of injury
How do you grade severity of TBI
GCS
What are the eye ratings in GCS
Eyes open spont (4)
Open to verbal command (3)
Eyes open to pain (2)
No eye opening (1)
What is the Verbal rating for GCS
Oriented (5)
Confused conversation/ can answer questions (4)
Inappropriate responses (3)
incomprensible sounds or speech (2)
No verbal response (1)
Motor response for GCS
Obeys command for movement (6)
Purposeful movement (5)
Withrdrawls from pain ( 4)
Spastic decorticate posture (3)
Decerebrate posture (2)
No motor response (1)
A GCS of 13-15 is…
Minor brain injury
What is a GCS of 9-12…
Moderate brain injury
What is a GCS of 3-8 ..
Severe Brian injury
A pt presents with a brief LOC, and within minutes is fully alert with nausea, difficulty concentration, mild blurred vision
GCS of 13-15
What is this ?
Concussion
What is the CT criteria for a mTBI
Persistent severe HA
Repeated vomiting (two or episodes)
Severe MOI (speed over mph)
Underlying coagulopathy
Age > 65 years
> 30min of retrograde or persistent anterograde amnesia
Intoxicated
What is Post Concussion Syndrome
Post-concussion syndrome is the sequelae of a mTBI/concussion that is defined by the continuation of symptoms of headache, dizziness, and cognitive impairment.
A mild traumatic brain injury is a mild injury to the brain caused by a blunt force or shaking of the brain inside of the skull.
What is the diff between Post Concussion Syndrome Vs Post Concussion Disease
PCS: symptoms that continue seven to 10 days after the initial injury
PCD: > 3 months
A pt presents with a GCS 9-12
What is the Tx approach
Admit for Mod/Int TBI
Head CT
may find contusion or hematoma
A pt has a concussion with S./s that persist beyond 6 days is termed
Post Concussion Syndrome
Describe Epidural Hematoma
Typically present as
- Trauma
- Progressive coma
- lucid intervals
Most common cause is a trauma to the middle meningeal artery
Suspect in a patient with temporal skull fracture
Classic CT finding: Convex hyper-density o/s brain tissue in the pariotemporal region
Mortality is 100% if left untreated
Get urgent CT scan
Describe Subdural hematoma
Accumulation of blood in the subdural space
Bleeding is from the cerebral vasculature
Blow from front or back or when skull hits fixed object (windshield)
Bridging veins between the dura and the arachnoid are torn when the two separate
Chronic in the elderly
Define Coma
deep sleeplike state with eyes closed from which the patient cannot be aroused
Define Stupor
higher degree of arousability in which the patient can be transiently awakened by vigorous stimuli, accompanied by motor behavior that leads to avoidance or withdrawal from uncomfortable or aggravating stimuli.
Define Drowsiness
simulates light sleep and is characterized by easy arousal and the persistence of alertness for brief periods.
What are the most important brainstem reflexes
Pupillary signs
Ocular movements
RR patterns
What are the three cardinal features of brain death
Coma/unresponsiveness
-No response to painful stimuli
Absence of brainstem reflexes
-Pupils, oculocephalic, gag, grimacing
Apnea
-No respiratory attempts even with PCO2 > 60mmHg
Define meningitis
Inflammation of the leptomeninges.
Caused by infection: viral, bacterial, fungal, or other.
Headache is a prominent feature: pain due to inflammation of intracranial pain sensitive structures.
What is the classic triad in meningitis
Fever
HA
Nuchal Rigidity
What are the classic CSF abnormalities
(1) polymorphonuclear (PMN) leukocytosis (>100 cells/μL in 90%),
(2) decreased glucose concentration (<2.2 mmol/L [<40 mg/dL] and/or CSF/serum glucose ratio of <0.4 in ~60%),
(3) increased protein concentration (>0.45 g/L [>45 mg/dL] in 90%),
(4) increased opening pressure (>180 mmH2O in 90%).
What is the Tx approach to Menigitis
Age 1-3 months: ampicillin + Ceftriaxone
Age 3 mon to 55 y/o Ceftriaxone PLUS Vanc
Alcoholism/? Ampicillin +Ceftriaxone +Vanc
Impaired cellular immunity
- ampicillin plus Ceftazadime plus Vanc
What is the characteristic rash for N. Minigitidis
Purpuric rash
What time frame should you give ABX for meningitidis
Within 60 min of admin
What is the MC cause of viral meningitis
Enterovirus
A pt CSF has increased cell count
With normal protein concentration
With normal gl and normal opening pressure
With S.s of menigitis
Think
Viral
What are the common cause of encephalitis
Herpesviruses: human to human transmission
Herpes simplex 2, Varicella-zoster, Epstein-Barr virus
Enterovirus: fecal-oral transmission
Arboviruses: mosquitoes, ticks (ie West Nile)
What are the important labs for Encepahlitis
Head Ct before LP to R/o
- Elevated intracerebral pressure (ICP)
- Obstructive hydrocephalus
- Mass effect
MRI and EEG and eval the CSF
What is the general approach to Encephalitits
Appropriate management of the airway
Fluid and electrolyte balance
Nutrition
Avoid and treat secondary infection
Treat hyperpyrexia (fever) Manage ICP -Head elevation -Diuresis -Mannitol -Seizure precautions
What is the pathogenesis of Migraine
Trigeminovascular system
Serotonin
Dopamine
Inherited
Define Migraine without aura
A lead 5 attacks that:
Last 4-72 hours with at least 2 of the following
Unilateral location
Pulsating quality
Moderate or severe intensity
Aggravation by or causing avoidance of routine physical activity (e.g., walking, climbing stairs)
During the headache they have at least Nausea, vomiting, or both
Photophobia and phonophobia
Define Migraine with aura
A least 2 attacks with one or more of:
reversible aura symptoms:
Visual, sensory, speech and/or language, motor, brainstem, retinal
With at least 2:
One aura symptom spreads gradually over ≥5 min, and/or two or more symptoms occur in succession
Each aura symptom lasts 5-60 min
At least one aura symptom is unilateral
The aura is accompanied, or followed within 60 min, by headache
What does POUNDING stand for
Pulsatile Onset/duration: 4-72 hours Unilateral in location Nausea and vomiting Disabling in intensity: headache is moderate to severe
What defines chronic headache
8 or more days per month
AND
At least 15 total days of HA per month
What are the DOC for acute mild migraine attacks
Simple Analgesics
Acetaminophen, aspirin, caffeine (Excedrin Migraine) Two tablets or caplets q6h (max 8 per day)
NSAIDs
Naproxen (Aleve) 220–550 mg PO bid
Ibuprofen (Advil, Motrin) 400 mg PO q3–4h
Tolfenamic acid (Clotam Rapid) 200 mg PO; may repeat ×1 after 1–2 h
Diclofenac K (Cambia) 50 mg PO with water
What is Ergotamine used for
Non selective Stimulating Seretonin receptor
Start at first sign of migraine
When do you give triptans in Migraines
AFTER THE AUREA
Triptans can be combined with what other medication to reduce HA recurrence
Combine with naproxen
What are the two most efficacious Triptans
Rizatriptan and Eletriptan are most efficacious
What is the role of using dopamine receptor antagonist in Migraines
Adjunctive therapy
Improves gastric motility –
improved absorption of other meds
Relieves nausea
When would you start using metoclopramide or prochloperazine
Pts w/
-increasing frequency
-Attacks unresponsive or poorly responsive to abortive treatments
-4 or more attacks per months
Takes 2 to 12 weeks before an effect is seen
What is the only proven drug for Tension headache prophylaxis
Amitryptyline
