Neurology Flashcards
In-class review for exam
Glasgow Coma Scale Mnemonics: VOICE Obeys .... 44 ....
VOICE for Verbal Response
V: voiceless (1) - O: ooohhh incoherent (2) - I: inappropriate words (3) - C: confused but answers (4) - E: elegant speech (5)
Obeys… for Motor Response
Obeys (6) → Localizes pain (5) → Draws from pain (4) → Bends (3) → Extends (2) → None (1)
44…for Eye Opening Response
44- open eyes = spontaneous opening (4)
3- lips = verbal/speech makes eyes open (3)
2- pointy = ouch open eyes from pain (2)
1- sideways looks like closed eyes no opening (1)
ID the type of hematoma: WITH a lucid interval? WITHOUT a lucid interval? \+ ID anatomic location of blood
WITH lucid interval: Epidural Hematoma
-Above the dura mater (lentiform)
WITHOUT lucid interval: Subdural Hematoma
-Below the dura mater/above arachnoid matter (crescent)
55 y.o. smoker w/ hx of HTN, atherosclerosis, & etoh intake experienced a sudden LOC & a sudden severe HA
…
What should be a top differential
Subarachnoid Hemorrhage
d/t
Ruptured Saccular (Berry) Aneurysm
Normal intracranial pressure vs. Fatally high intracranial pressure
Normal: < 10-15 mmHg
Fatal: > 25-30 mmHg
Indications for ICP Monitoring
- Inability to follow commands or localize a stimulus
- Multiple systems injured + altered LOC
- Sedated patient (d/t inability to monitor their mental status)
- Known concurrent tx that elevates ICP
- Traumatic intracranial mass
- Acute fulminant liver failure + INR > 1.5 + Coma
* In general never do it in a pt who is awake & has normal neruo exam
Treatment for elevated ICP
- Raise HOB 30-45°
- Normotensive (keep BP normal)
- Hyperventilate
- Sedation
- Mannitol
- Hypertonic saline
- Control hyperglycemia
- Seizure prophylaxis
Transient altered mental status d/t a diffuse traumatic brain injury
-Pathophys: d/t what type of crisis?
-List the “no-go” characteristics & also generally reasons to go to the ER
-
Concussion
- Pathophys: Energy crisis from shearing of axons
- “No-go”: LOC, Seizure, Fencing, Gross Motor Instability, Confusion, Amnesia, *repeated N/V
Sample Question:
Unidentified male s/p MCC. On arrival to ER, the pt is confused, but able to respond to questions appropriately. He is groggy, but opens his eyes to verbal command and is able to make purposeful motions in response to painful stimuli. Glasgow Coma Score (GCS)?
12
Second Impact Syndrome
-Definition
Rare Phenomenon when diffuse cerebral swelling develops in the setting of a second head trauma (any severity) occurring while a pt is still symptomatic from a previous concussion, can be deadly
At risk for this if pt is undergoing active litigation, repeat concussions, GCS < 13 on presentation. Generally pt might have chronic HA, difficulty w/ memory, fatigue, sleeping challenges, personality changes, sensitivity to light/noise.
-Tx?
Post-concussion Syndrome Tx: -Rest, both PHYSICAL & COGNITIVE -Symptomatic tx of HA & mood sx -+/- referral for neuropsychological testing
In a suspected traumatic brain injury, when is it ideal to perform a Glasgow Coma Scale evaluation? Should be followed up by what?
Within 30 minutes of the injury
+
MRI or CT scan
What does Golden Hour refer to?
In TBI’s it is essential to treat within the first 60 minutes of presentation! Improves mortality.
Define the following Skull Fractures:
- Linear
- Depressed
- Diastatic
- Basilar
Linear: break to skull w/o movement (*mc temporoparietal, frontal, occipital)
Depressed: sunken spot
Diastatic: fx along a suture line & it pries apart
Basilar: fx at base of skull (*most serious)
(+) Racoon Sign or battle sign
Basilar skull fx
Post skull fx, note clear fluid on pts pillow, it could have been from their nose or ear, you suspect…
Basilar skull fx
MC artery ruptured in an Epidural Hematoma
Middle Meningeal Artery
Arterial blood + above dura + lucid for several hrs + craniotomy if > 30 cm^3
Epidural Hematoma
Venous blood + below dura + NOT lucid + fall or MCV or assault
Subdural Hematoma
What is it called when an elderly pt has a subdural hematoma that progressively presented w/ sx
SUBACUTE subdural hematoma
Caused by an injury to vasculature of the brain
- Presentation?
- Can be fatal if ICP is at what value?
- Treatment?
Subarachnoid Hemorrhage or Brain Herniation
Presentation: Sudden, severe HA, +/- focal neural deficit, ↑ BP
Fatal ICP if > 25-30 mmHg
Treatment:
-Control BP
-Surgical: clipping or wrapping aneurysm or catheter to remove embolization
Prognosis for Subarachnoid Hemorrhage
⅓ survive + good recovery
⅓ survive + disability
⅓ die
Repetitive mild head injury
Observed in athletes or military personnel
Tau degenerative change at superficial cortical layer of brain
Cognitive, behavioral, mood sx
Supportive tx only
Chronic Traumatic Encephalopathy
AEIOU TIPS
Possible causes of Dementia A: alcohol or AAA E: electrolytes or endocrine I: insulin/blood sugar O: opiates U: uremia T: trauma, temp or toxemia I: infections (sepsis, meningitis) P: psychogenic or pulmonary embolus S: space occupying lesion/strokes/shock/seizure
3 assessments for Altered Mental Status suspected to be from damaged brainstem function
- Corneal Reflex
- COWS
- Doll’s Eyes
Always consider these 3 reversible causes of Altered Mental Status
- Hypoglycemia (check glucose → +/- give dextrose)
- Opiate overdose (trial of naloxone)
- Thiamine deficiency (trial of thiamine)
AVPU Scale
Assess Altered Mental Status A: alert V: verbal P: pain U: unresponsive
Definitions:
- Confusion
- Drowsiness
- Lethargy
- Stupor
- Coma
- Delirium
Confusion
Behavioral state of ↓ mental clarity, coherence, comprehension, reasoning
Drowsiness
Patient not easily aroused by touch or noise, cannot maintain alertness for some time
Lethargy
Depressed mental status, pt can appear wakeful but w/ ↓ awareness of self/environment/globally, cannot be aroused to full function
Stupor
Takes vigorous stimuli to wake the pt, and pt does put in an effort to avoid uncomfortable or aggravating stimulus
Coma
Unable to arouse pt by stimulation, and pt DOES NOT put in an effort to avoid painful stimuli
Delirium
Acute onset of fluctuating cognition w/ impaired attention & consciousness, ranges from confusion → stupor
Method to assess Delirium
CAM
Confusion Assessment Method
Acute confusional state
Transient global disorder of attention + clouding of conscience
Delirium
These are all types of what?
- Sundowning
- ICU psychosis
- Terminal
Delirium
MC cause of delirium in hospitals?
Other causes in general?
Hospitals: Withdrawal (etoh or substance)
General: Systemic problem (meds, hypoxemia, infection)
Which one has a primary deficit in ATTENTION?
Dementia or Delirium?
Delirium
Attention deficit Rapid onset + Fluctuating Anxiety Irritability HYPO or HYPER reactive
Delirium
Delirium
Treatment
- Prevention
- ID underlying cause & resolve it
- Remove offending factor, like medication (especially opioids) - Significant behavioral control issues + Subjective distress → Haloperidol
Delirium
Prognosis
- Typical 1 week duration
- Full recovery (usually)
- Some never return to baseline
- Associated w/ worse clinical outcomes overall
Progressive decline in INTELLECTUAL function w/ loss of short term memory + 1 additional cognitive deficit
-What stays preserved?
Dementia
Preserved: Attention/Motor function/Speech
All pts > 70 y.o. must receive a Screening Mental Exam to ID what?
Dementia
*50% of ppl > 85 y.o. have Dementia
Irreverisble vs. Reversible causes of Dementia
Irreversible causes:
Alzheimer’s, vascular dementia, Creutzfeldt-Jakob dz
Reversible causes:
Depression, vit B12 deficiency, syphilis, hypothyroidism, NPH, drug use, intracranial mass
Dementia
Treatment
- Depression Screening
- Aerobic Exercise Daily
- Frequent Mental Stimulation
* Unlikely to regain lost skill s
Early loss of short term memory, a neruodegenerative dz, variable deficits of executive function, visuospatial function, & language
Alzheimer’s
MC age related neurodegenrative dz
Alzheimer’s
2nd MC age related neurodegerative dz
Parkinson’s
ß-amyloid peptide plaques + neurofibrillary tangles w/ tau protein
Found throughout the neocortex
Cholinergic deficiency → memory, language, visuospatial changes
Alzheimer’s
Alzheimer’s Sx
1st Sx → steady progression of SHORT term memory loss
Progresion to → long term memory loss, disorientation, behavioral & personality changes
↓ intellectual function & cognition
Mental Status Exam shows intellectual decline in > 2 ares of cognition
Alzheimer’s
Alzheimer’s
Treatment
Cholinesterase Inhibitors: Donepezil, Rivastigine, Galantamine Tacrine
NMDA Antagonist: Memantine (MOD-SEVERE Alzheimer’s)
Best combo: Cholinesterase Inhibitor + NMDA Antagonist
*SAME tx in lewy body dementia
Cognitive, dysfunction, neruodegenerative dz, variable deficits of executive function, visuospatial function, hallucinations & language w/ onset earlier in life
Lewy Body Dementia
Lewy Body Dementia
Sx
Psychiatric disturbance + … →Anxiety w/ visual hallucinations →Fluctuating delirium Parkinsonian motor defects 80% have hallucinations
Histologically indistinguishable from Parkinson’s
α-synuclein containing Lewy bodies occur at brainstem, midbrain, olfactory bulb, & the neocortex
Lewy Body Dementia
Excess CSF accumulating in the ventricles possibly linked to PMHx of head injury
Normal Pressure Hydrocephalus
Normal Pressure Hydrocephalus
Sx
Gait apraxia (magnetic gait)
Urinary incontinence
Dementia
Diffuse disease of the brain that alters brain function or structure
Rare in humans
Invariably fatal
-Which is the most common?
Prion Disorder
-MC: Sporadic Cretzfeldt-Jakob Disease
Cognitive decline Myoclonic fasciculations Ataxia Visual disturbance Pyramidal & extrapyramidal sx Variant type found in young people w/ prominent psychiatric or sensory loss
Prion Disorder
The only drug that can help with cognitive decline in a Prion Disorder, but ultimately does not at all help the progression toward death.
Flupirtine (analgesic)
→Possibly slows cognitive decline
Wernicke’s Encephalopathy
- Definition
- MC cause in US
- Sx (3)
- Tx
Wernicke’s Encephalopathy
- Definition: degenerative brain disorder d/t lack of thiamine (B1)
- MC cause in US: Alcoholism
- Sx: 1. Confusion 2. Ataxia 3. Ophthalmoplegia/nystagmus
- Tx: Thiamine 100 mg
Any combination of tremor, rigidity, bradykinesia, & progressive postural instability
+/- cognitive impairment
Parkinsons Disease
Required: Bradykinesia + 1 additional cardinal feature of TRAP
….
Like what & for what ctn?
Tremor Rigidity Akinesia Postural instability for Parkinsons
How are the following Parkinson’s meds prescribed for the situations below…
Meds: Selective MAOI, Amantadine, Dopamine Agonist, Levodopa
Scenarios: Mild Sx: > 70 y.o. + severe motor deficit: Young patient: Mild/need to potentiate levodopa:
Mild Sx: →Amantadine (old tx probs not used anymore) > 70 y.o. + severe motor deficit: →Levodopa Young patient: →Dopamine agonist + Levodopa Mild/need to potentiate levodopa: →Selective MAOI
After suffering a severe TBI how likely are you to develop Parkinson’s?
45% MORE likely than the average person
Dopamine depletion from degeneration of the dopaminergic nigrostriatal system/ substantia nigra pars compacta → imbalanced dopamine & acetylcholine
Parkinsons Disease
What are the most minimal requirements to make a clinical diagnosis of Parkingsons
Required: Bradykinesia + 1 additional cardinal feature of TRAP
Pill Rolling Resting Tremor
Parkinsons
Postural tremor that emerges when performing an action (not present at rest)
…
Is most likely what?
What is a treatment?
Essential Familial Tremor
Tx:
Propranolol
CAG trinucleotide repeat
- What inheritance?
- What is its classic motor abnormality?
- Prognosis?
Huntington’s
- Inheritance: Autosomal dominant (Chromosome 4)
- Chorea
- Pt dies 15-20 yrs after onset of clinical sx
Degeneration at anterior horn cells of spinal cord, motor nuclei of the lower cranial nerves, & at the corticospinal & corticobulbar pathways
+
3 regions of denervation & spontaneous resting muscle activity
Amyotrophic Lateral Sclerosis
- Must have 3 regions of changes on Electromyography:
1. Cervica. 2. Throacic 3. Lumbosacral
Riluzole
- Treats what ctn?
- What supportive tx must accompany it?
- Prognosis?
Amyotrophic Lateral Sclerosis *riluzole is a glutamate blocker fyi Supportive: \+/- non invasive ventilation \+/- assertive devices \+/- physical therapy
Prognosis:
Fatal, in 3-5 yrs of onset
Multiple motor or phonic (or both) tics
Onset typically prior to 18 y.o., MC between ages 2-15 y.o.
Tx?
Tourette Disorder
Preceded by an urge & relieved by performance
Tx:
Cognitive Behavioral Therapy
Clonidine (α-agonist)
This disorder involves motor & phonic function that occurs b/c pt cannot resist the urge & the urge is resolved by performing
+
Tx
Tourette Disorder
α-agonists: Clonidine Other: Tetrabenazine, RisperidoneHaloperidol Fluphenazine or Pimozide Motor/facial only: Botox injection Deep brain stimulation
CNA immunoglobulin production + altered T lymphocytes characterized by inflammation w/ multiple foci of demyelination in CNS + HLA DR2/↓ Vit D/Smoker
-What ar the MC ages of onset?
-
Multiple Sclerosis
Reactive gliosis
Multiple Sclerosis
-Damage from the CNS insult & demyelination cause glial cells to hypertrophy
4 types of MS
Relapsing-remitting: Exacerbation & remission cycles Spontaneous \+/- triggered by infection Primary progressing: Gradual progression w/o remission \+/- temporary plateaus Secondary progressing: Starts like relapsing-remitting then turns into gradual progression Progressive relapsing: Progresses gradually → sudden, clear relapses interrupt
Multiple Sclerosis
Symptoms
Paresthesias in > 1 extremity or on the Trunk or on 1 side of the Face
Weakness, numbness, tingling, unsteadiness on a limb
Lhermitte’s sign: electric shock sensation in limbs & torso after movement of neck
Uhthoff’s phenomenon: worsening symptoms w/ heat
Lhermitte’s Sign
electric shock sensation in limbs & torso after movement of neck
from MS
Uhthoff’s Sign
worsening symptoms w/ heat
from MS
2 ways of diagnosing MS w/ MRI imaging
> 2 CNS lesions/plaques for dx
Single pathologic lesion w/o explanation for the finding
→Clinically Isolated Syndrome (CIS) dx
→F/U MRI in 6-12 m.o. to assess any new lesions
Acute Relapse:
Corticosteroids → Methylprednisolone IV (TID) → Prednisone PO (1wk + 2-3 wk taper)
Prevention of a Relapse:
Immunomodulation
Spasticity:
Baclofen or tizanidine
Pain:
Gabapentin or TCA (like amitriptyline) or carbamazepine or opioids
Severe, intractable:
Plasma exchange, hematopoietic stem cell transplant
Fatigue:
Amantadine, modafinil, armodafinil, or extended release amphetamine
Behavioral modifications
….
What is this tx for? What is its goal?
Multiple Sclerosis
Goal: preventing relapses + ↓ accumulation of disability
Fluctuating weakness of commonly used voluntary muscles
Diplopia, ptosis & difficulty swallowing
Activity increases weakness of affected muscles
-What can improve ptosis?
-Pathophys?
-3 diagnostic tests?
Myasthenia Gravis
- Ice Test
- Auto-antibodies vs. acetylcholine receptors (↓ # functional receptors)
- Ab vs. receptors 2. LDL receptor related protein 3. Tensilon Test/Edrophonium Test
Myasthenia Gravis
Treatment
- Neurology referral
- Neostigmine/Pyridostigmine (anti-cholinesterase-short acting)
- Thymectomy
- Unresponsive to -stigmines or surgery: Corticosteroids (prednisone)
- Refractory: mycophenolate mofetil/cyclosporine
- Major disability or Myasthenic crisis: Plasmapheresis/IVIG therapy
Thymoma + Myasthenia gravis =
MC in older men
Group of CNS disorders associated to Muscle Tone, Strength, Coordination, Postural Abnormalities d/t injury at the perinatal or prenatal period
- Sx?
- Tx?
Cerebral Palsy Sx: Spasticity (75%) Motor deficit: Hypotonia, fine motor difficulty, ataxia, dystonia Tx: Supportive
Urge to move legs + immediate relief after moving legs or walking
- What should be part of the workup?
- Tx?
Restless Leg Syndrome
- Workup: Iron deficiency
- Tx: Pramipexole, ropinirole (dopamine agonists)
Muscular Dystrophy
-Definition
-MC type, 2nd common type
(general patho)
Progressive muscle WASTING & WEAKNESS
MC: Duchenne (ABSENCE of dystrophin)
2nd common: Becker (ABNORMAL dystrophin)
Pt w/ hypertrophied calf muscles + inability to climb up their stairs at home + intellectual disability
- Dx?
- 2 tests that can support your dx?
- Tx?
Dx: Muscular Dystrophy
L/T:
1. CK: ↑ if d/t Duchenne or Becker MD
2. Muscle Bx: (+) muscle wasting
Tx:
- Eteplirsen (dna modulation)
- Corticosteroids
NF1 gene mutation on Chromosome 17
vs.
NF2 (Merlin) gene mutation on Chromosome 22
Nerurofibromatosis
Chromosome 17 = Type 1 → neurofibromas anywhere on the body/skin
Chromosome 22 = Type 2 → neurofibromas on CN 8 or intracranially/intraspinally
Sensory: hyperalgesia, &/or allodynia (sensory stimulus worsening pain)
Vasomotor: skin, temperature, color asymmetry
Sudomotor/edema: edema, sweating changes, or sweating asymmetry
Motor/trophic: ↓ ROM or motor dysfunction &/or trophic changes (hair, nail, skin)
…
With this information, how can someone get dx w/ Complex Regional Pain Syndrome?
Limb Pain + >/= 1 sx from 3 of 4 categories listed
CLASSIC TRIAD:
- Burning pain
- Autonomic dysfunction
- Trophic changes
Non dermatomal limb pain after trauma or surgery w/ sensation of burning pain, autonomic dysfunction, & trophic
-Tx?
Complex Regional Pain Sydnrome
Tx:
NSAIDs
Prednisone
Gabapentin
Shoulder-pain syndrome
Hand + Ipsilateral ROM of shoulder w/ Complex Regional Pain
- **MC in hand
- **This syndrome can also occur
Gullian-Barre Syndrome
Definition
-MC post infectious care
-Most significant iatrogenic cause
Acute immune-mediated progressive polyneurophathy + progressive muscle weakness
- Campylobacter jejuni infx
- Post-immunization
Ascending progressive & often symmetric muscle weakness (legs → arms) + ↓ reflexes+ acute polyneuropathy
- Dx?
- 2 diagnostic criteria
- Serology finding?
- Tx?
Gullian-Barre
2 Diagnostic Criteria:
- Progressive weakness of legs & arms
- a-reflexia or ↓ reflexes in weak limbs
Serology: (+) antibodies for glycolipid Gl1b
Tx: #1: Plasmaphoresis #2: IVIG
Gullian Barre:
- When can someone have a vaccine?
- General functional prognosis at 1 yr?
- Deadly complication?
After 1 year → immunizations should be considered on an individual basis
At 6 m.o. 80% of ppl can walk
Paralysis of chest muscles/diaphragm → respiratory failure
Pain, burning, tingling at hand during sleep
- Dx
- Sx anatomic distribution?
- What PE tests would be (+)?
- Non pharm tx?
- If sx persist > 12 m.o.?
Carpal Tunnel Syndrome
Median Nerve Innervation:
1st 3 digits + radial ½ of the 4th digit
Splint at neutral 30° flexion for < 3 m.o.
Carpal tunnel surgical release if sx persist x > 12 m.o.
2 significant Risk Factors
Duration & severity of hyperglycemia
Glycemic variability
…
For what condition?
Diabetic Peripheral Neuropathy
5.07 Semmes-Weinstein Monofilament Test
Used to ID Diabetic Peripheral Neuropathy
MC complication of DM2
Diabetic Peripheral Neuropathy
Hyperglycemic oxidative stress leading to neuronal damage + symmetric distal sensory loss (burning/weakness) + worse at night
- Dx?
- Tx?
Diabetic Peripheral Neuropathy
Tx: (TCA’S)
Nortriptyline
Desipramine
Screening Indications for Diabetic Peripheral Neuropathy
DM2 at Diagnosis
DM1 at 5 yrs post-diagnosis
Prediabetics w/ sx
SUBSEQUENTLY to 1st screening must repeat Q-annually
Method of screening for Diabetic Peripheral Neuropathy
Thermal or Pin Prick (small nerve function)
Vibration, proprioception, monofilament, DTR at ankle vs more proximal locations (large nerve function)
Michigan Neuropathy Screening Test
> 4 Points → Neuropathy
PE Score >/= 2.5 indicated sc of neuropathy
Rocker bottom foot
Diabetic neuropathic arthropathy (charcot foot)
Collapse of the medial arch
Medial convexity
Deformity caused by displacement of the talo-navicualr joint & tarsometatarsal dislocation
Unilateral warmth, redness, & edema over the foot/ankle + DM
…
Always r/o what?
Tx?
Diabetic neuropathic arthropathy (charcot foot)
Tx: Non-weight bearing + cast 3-25 m.o. (non-removable cast) 3-26 mo.o (removable cast) Manage inflammation Podiatry for footwear Surgery
Wide spectrum of manifestation affecting different orang systems
Secondary to DM
Systems:
GI, CV, GU, pupillary, sudomotor, neuroendocrine
Sx: GERD, Gastroparesis, Chronic Diarrhea
DIABETIC AUTONOMIC NEUROPATHY
Severe shoulder pain followed within days of weakness, reflex changes, sensory disturbances at the distribution of C5/6 Wasting of affected muscles d/t: Idiopathic Trauma Including at time of vaginal delivery Resulting from a congenital anomaly Neoplastic
BRACHIAL PLEXUS NEUROPATHY
2 types of Bell’s Palsy
CN 7 palsy
Central: Preserved ability to frown Eye unaffected (+) mouth drooping Peripheral: Inability ability to frown Ptosis (Eye affected) (+) mouth drooping
Essential in diagnosing someone with Bell’s Palsy +Tx?
Rule out other causes, especially stroke
Tx:
High dose Prednisone x 1 week
Trigeminal Neuralgia (CN 5)
Causes (2)
Sx
Tx
Causes: 1. neighboring vessel compression 2. underlying ctn like MS
Sx: Sudden stabbing/lancinating facial pain
Tx: conservative, like carbamazepine
Which CN causes:
Defect in smell (ansomia)
CN 1
Which CN causes:
Impaired vision
CN 2
Which CN causes:
Out & down tilt of eye
CN 3
Which CN causes:
Up & in tilt of eye
CN 4
Which CN causes:
Inward tilt of eye
CN 6
Which CN causes:
Absent corneal reflex/anestheisa of forehead
Anesthesia of midfac e
Jaw deviation toward lesion
CN 5
1
2
3
Which CN causes:
Horizontal diplopia
CN 3 & 6
Which CN causes:
Vertical diplopia
CN 4
Which CN causes:
Sensorineural hearing loss, horizontal nystagmus, vertigo
CN 8
Which CN causes:
Posterior 1/3 of tongue w/o taste or sensation, no sensory at soft palate/upper pharynx, flaccid paralysis of soft palate, uvula deviates away from lesion
CN 9
Which CN causes:
Epiglottic paralysis, flaccid paralysis of soft palate w/ uvula pointing away from lesion, vocal cord issues, stomach gastroparesis
CN 10
Which CN causes:
Sternocleidomastoid paresis
Trapezius paresis
CN 11
Which CN causes:
Tongue atrophy
Fasiculation of tongue
CN 12
Unilateral periorbital pain > 15 min + 1 of the following:
Ipsilateral nasal congestion or rhinorrhea, or lacrimation or redness of eye
Horner syndrome (ptosis, pupillary meiosis & facial anhidrosis or hypohidrosis)
Tx in ER setting:
Cluster HA
ER:
100% O2 12-15 L x 15 minutes
+- Triptans
