Test #2 Flashcards
Upper Motor Neuron lesion vs Lower Motor Neuron lesion
Upper motor neuron lesions may have both ipsilateral and contralateral manifestations due to decussation in the pyramids
Lower motor neurons are entirely ipsilateral
Bell’s Palsy is a LMN lesion
Extremely high CPK DDx
Muscular dystrophy
Thyroid disease
Complete lesion
Total or partial extremity loss
Paraplegia, quadriplegia
Incomplete lesion:
Anterior cord syndrome
Central cord syndrome
Brown-Sequard Syndrome
Depends on the part of the cord injured
Anterior = flexion injury; lose motor, pain, temperature
Central = ischemia or hemorrhage; UE affected more than LE
- reverse paraplegia
Brown-Sequard = penetrating injury on one side causes motor loss to that side and sensory loss on the other side
DTR’s and nerve roots
Biceps: C5, C6
Brachioradialis: C6
Triceps: C7
Patellar: L4
Achilles: S1
Muscular Dystrophy
Progressive loss of muscle tissue
Causes progressive weakness, drooling, ptosis, problems walking
Concussion Pathophysiology
Neuronal depolarization with excitatory neurotransmitters released - potassium and calcium influx
Get impaired glucose metabolism, cerebral blood flow, axonal function
Initial TBI Evaluation
Mental status: Orientation, concentration/cognition, memory
Gait and balance assessment: Rhomberg
Concussion Signs of an Emergency
Increasing HA
N/V
Progressive consciousness impairment
Gradual BP rise
Diminution pulse rate
Blown pupil
Disorientation
Emergent TBI Referrals
Suspected hematoma
C-spine injury
Worsening LOC
Focal motor weakness
Transient quadriparesis
Seizure
TBI Non-Emergent Referrals
Persistent HA >7days
Post-concussion syndrome >2 weeks
Abnormal neuropsych testing
Hx multiple, high-grade concussions
USE YOUR CLINICAL JUDGEMENT
Disorders that concussions may mimic
Substance Abuse/Dependency
Intermittent Explosive Disorder
Suicidal Ideation/Tendencies
Depression/Mood Disorders
Impulse Control
Indications for Emergent Transfer to ER (Athletic injuries)
LOC
Possible C-spine deformity or skull fracture
High risk for ICH
Post-traumatic seizure
Worsening mental status
Mild Concussion Treatment
Physical and Cognitive (no TV/phone) rest
- allow to sleep
Avoid NSAIDs 1st 48 hours post-injury
No recreational activity w/ head injury risk until healed
Return to Play/Rule of 3’s
Return to play according to where they are on rule of threes
May slowly work up to full contact with several baby steps to put off full contact
Rule of 3’s
1 concussion = sit out rest of the game
2 concussions = sit out rest of season
3 concussions = end of that sport
Second Impact Syndrome
Metabolic cascade causing sudden, severe swelling
May be minor or worsen to mental status which will progress to death
Post-Concussive Syndrome
Chronic cognitive and behavioral symptoms following injury
Can take months to recover, watch for depression
Sx: HA, fatigue, sleep issues, emotional and concentration problems, dizziness
Tx: Physical and Cognitive rest, physical therapy
No long-term issues once healed
Chronic Traumatic Encephalopathy
Progressive degenerative disorder in pts w/ hx of multiple concussions or head injuries
Sx: Memory loss, confusion, impaired judgement, paranoia, impulse control, aggression, depression, progressive dementia
Can only Dx on autopsy -> Tau protein in the brain
Dysarthria
Problems with the muscles that produce speech
Dysconjugate gaze
Failure of the eyes to turn together in the same direction
Apraxia
Difficulty with the motor planning to perform tasks of movement when asked
Do they know how to start? Can they follow two-step instructions
Dystaxia
Lack of muscle coordination
Agnosia
Inability to process sensory information
Loss of ability to recognize objects, persons, sounds, shapes, smells
FAST campaign
Facial droop
Arm weakness
Speech difficulties
Time to call 911
Brainstem Cranial Nerves Housed:
Midbrain: 3,4
Pons: 5,6,7,8
Medulla: 9,10,11,12
TBI Features that indicate ICH
Worsening HA
Confusion
Lethargy
Diffuse Axonal Injury
Indirect trauma
Axonal neurofilament disruption causing impaired thought and axonal swelling
-Shaken baby syndrome, severe whiplash
Reading a Head CT scan
Look at cranial contours
Look for lesions; type and location
Look to see if cisterns are open or closed
Check for midline shift
Acute blood = white, older blood is darker
Open Skull Fracture
Overlying scalp lac with disrupted dura OR
Fracture through a paranasal sinus or middle ear
Life-threatening Headache DDx
Subarachnoid hemorrhage
Bacterial meningitis
Cerebral ischemia
Subdural hematoma
Brain tumor
Decorticate posture indicates damage in:
Cerebrum
Internal capsule
Thalamus
Decerebrate posturing indicates damage in:
Uncal herniation -> brainstem damage
Poor prognosis
Seizure Treatment - 1st and 2nd line
1st line: Benzodiazepines - terminate ictal activity
2nd line: Phenytoin and Phenobarbital
Distinguishing Vertigo
Peripheral: N/V, recurrent, lasts 2-3 hours max
- positional, vestibular neuritis, herpes zoster, Aminoglycoside toxicity
Central: gait disturbances, lasts hours to days
- Migraine, brainstem ischemia, cerebellar infarct or hemorrhage, MS
Determining TIA Cause
Low flow: Internal carotid (US), MCA or vertebrobasilar (CT Angio)
Embolic: EKG/Echocardiograph looking for clots
Lacunar: r/o all other, Dx of exclusion
Positive Symptoms
Indicate active discharge from CNS neurons
Negative Symptoms
Indicate absence or loss of function
Symptoms that rule out Guillian-Barre Syndrome
Abrupt sensation demarcation
Prolonged asymmetry of weakness
Severe and persistent bladder/bowel dysfunction
>50 wbc in CSF
Stroke Distinction by Symptoms
ACA
MCA
Brainstem
Lacunar
ACA: Leg weakness and numbness, +/- mental changes
MCA: Aphasia, gaze deviation, cut visual field, face and arm weakness
Anterior bleed sx are always ipsilateral
Brainstem: Crossed findings (ipsilateral and contralateral), ataxia, eye movement/pupil dysfunction (CN)
Lacunar: Pure motor or pure sensory loss
NIH Stroke Scale
0 = No stroke
1-4 = Minor stroke
5-15 = Moderate stroke
16-20 = Moderate/Severe stroke
21-42 = Severe stroke
Rheumatic mitral stenosis associated w/ what type of stroke
Ischemic stroke
Lacunar Infarct
<5 cm lesions in penetrating arterioles of basal ganglia, pons, cerebellum, internal capsuel, thalamus, and deep white matter
-Lower morbidity and mortality
CT: Clean or punched out hypodense areas
May be caused by HTN
Aphasia
Difficulty processing language, speaking, understanding others, or reading/writing
No impact on actual intelligence
Global Aphasia
Most severe form of aphasia
Produces few recognizable words, understands no speech, cannot read or write
Anomic Aphasia
Cannot supply words for things they want to talk about
Poor writing ability
Nouns and verbs are hardest
Understand speech well, adequate reading skills
Broca’s Aphasia
Expressive aphasia
Speech output severely reduced; short utterances w/ less than 4 words
Reading and writing are also affected
Broca’s area supplied by superior division L MCA
Wernicke’s Aphasia
Receptive aphasia
Fluent, but meaningless spontaneous speech; pt is unaware of speech errors
Poor comprehension, writing, and reading as well
Wernicke’s area supplied by inferior division L MCA
Hemorrhagic strokes
Intracerebral Hemorrhage (ICH) - poorly controlled HTN
-arterial bleed into brain parenchyma; sx increase as hematoma increases
Subarachnoid Hemorrhage - trauma, ruptured AVM/aneurysm
- Thunderclap HA, bleed into CSF and area around brain
- Often only bleeds for a few seconds, high risk for rebleed
Tissue Plasminogen Activator (tPA) contraindications that aren’t bleeding
BP >185/110
Glucose <50
Platelet <100,000
INR >1.7 or PT >15 seconds
Heparin w/in 48 hours
NIHSS >25
Primary Headaches
90% all headaches
Usually start between 20-40 years old
Migraine, Tension-type HA, Cluster (least common)
Secondary Headache
Are caused by an underlying disease
Can be harmless or dangerous
Watch for red flags indicating that HA is dangerous
Dangerous: Infectious, Subarachnoid hemorrhage, Temporal arteritis, Intracranial pressure
Migraines
HA results from blood vessel dilation from trigeminal nerve innervation -> get PNS neuropeptide release
Usually unilateral; throbbing/pulsating pain w/ N/V
Photophobia or phonophobia
+/- prodrome (60%) or aura (25%)
Migraine w/ Brainstem aura
Uncommon form
7-20 yo, females
Vertigo, dysarthria, tinnitus, diplopia, ataxia, decreased LOC
-need two of above to make this Dx
Hemiplegic Migraine
Unilateral motor weakness
Severe HA, scintillating scotoma, visual field defect, numbness, paresthesia, aphasia, fever, lethargy, coma, seizures
Retinal, Vestibular, Menstrual migraines
Retinal: Rare, repeated monocular scotomata/blindness attacks < 1hour followed by HA
Vestibular: Episodic, vertigo in pt w/ migraine hx - no confirming test, Dx of exclusion
Menstrual: Migraine before/throughout menstruation
-usually 2 days before or 3 days after bleeding onset
Migraine without aura diagnosis
@ least 5 attacks fulfulling below criteria
- HA attacks between 4-72 hours long
- @ least 2: unilateral, pulsating, moderate-severe pain, avoidance of routine physical activity
- @ least 1 during HA: N/V, photophobia and phonophobia
Migraine with aura diagnosis
@ least 2 attacks fulfilling criteria below
- 1 reversible aura sx: Visual, Sensory, Motor, Speech
- >=2: >1 aura symptom gradually spread over 5 minutes, or >=2 symptoms occur in succession
- Each aura sx lasts 5-60 minutes, accompanied or followed (<60min) by a HA
- @ least 1 aura sx unilateral
Migraine Tx - 1st, 2nd, and 3rd line
1st: NSAIDs/ASA
2nd: Triptan
3rd: Triptan + NSAID
Tension-Type Headache (TTH) and Treatment
Band-like, bilateral, non-throbbing mild/moderate HA
Peaks @ 4th decade
TX: ASA/Tylenol/NSAIDS 1st line w/ relaxation techniques
2nd line: Add caffeine to 1st line meds
3rd line: Butalbital (Fioricet/Fiorinal)
Cluster Headaches and Treatment/Prevention
Middle-aged men
Unilateral, recurrent, severe HA around eye w/ eye sx
-watering, congestion, swelling, rhinorrhea, lacrimation
MRI w/o contrast
Tx: 1st line: SubQ Sumatriptan + 100% O2 NRB
Verapamil for prevention - 2-3 weeks for effect
Temporal Arteritis Brief and Treatment
50-70 yo, Scandinavian descent
Temporal HA w/ scalp tenderness, fever, amaurosis fugax
Tx: Prednisone 4-60 mg daily, low dose ASA
-Start tx before bx results to save eye function
Guillain-Barre Syndrome (GBS) and Treatment
Symmetric ascending muscle weakness with absent DTRs and dysantonia (tachy, HTN-HOTN, bradycardia)
Dx: LP -> increased protein, normal wbc
Tx: plasmapheresis or IVIG
Bell’s Palsy and Treatment
Acute peripheral facial palsy with decreased tearing
Tx: early, short-term glucocorticoids (w/in 3 days sx)
Recovery may be disorganized
Eye care: Eye drops, keep it shut
Myasthenia Gravis and Treatment
Progressive muscle fatigability - Abs to acetylcholine receptors (AChR-Ab)
2nd-3rd decade for women (estrogen); 6th-8th decade men
Tx: Pyridostigmine (anticholinesterase) + chronic and rapid immunotherapies
-SE: diarrhea, decreased HR, increased salivation
Polyneuropathies
Symmetric distal sensory loss with weakness or burning sensation
Stocking and glove loss; r/o spinal problem
Diabetic, Alcoholic, Vitamin B12 and E, Thiamine deficiency
Diabetic Neuropathy
Most common polyneuropathy in US
Glycosylation end products, sorbitol accumulation, increased oxidative stress
Loss of vibratory, reflexes, pain, touch, temp; altered proprioception
Tx and prevention: Tight glycemic control
Alcoholic Polyneuropathy
ETOH is a direct neurotoxin
Demyelination and shrinking of fibers (normal thiamine), plus axonal neuropathy w/ coexisting nutritional deficiency (thiamine/B12/Vit E)
Vitamin B12 Polyneuropathy
Need adequate absorption - IF from parietal cells to bind Cbl
Subacute degeneration of dorsal and lateral spinal columns
Tx: IM B12 injections: 2X weekly for 2 weeks, then weekly for 2 months - once levels restored, monthly for life if issue still exists
Vitamin E Deficiency
Spinocerebellar syndrome
Often chronic cholestasis and pancreatic insufficiency
Tx: Prescription oral doses of alpha-tocopherol
Thiamine Polyneuropathy
Dry Beriberi: Neuropathy w/ calf cramps, muscle tenderness, burning feet; +/- autonomic neuropathy
Wet Beriberi: High output CHF and neuropathy
Dx: UA and serum thiamine levels
Tx: 50-100 mg IV/IM/PO - give before glucose in unconscious to prevent encephalopathy
Meningitis Community-Acquired Bugs by Age and Nosocomial
S. pneumo, N. meningitis, Group B strep, H-flu, Listeria
Newborn-1 mo: Group B strep
1-23 mo: S. pneumo
2-18 yo: N. meningitis
Adults (>18): S. pneumo
Nosocomial: E. coli, Klebsiella, P. aeruginosa
Meningitis Triad and PE
Triad: Fever (>38/100.4), Nuchal rigidity, AMS
-Also get late stage non-blanching rash
Kernig sign: cannot extend leg w/ hip flexed while supine
Brudzinski’s sign: Spontaneous hip flexion w/ passive neck flexion
LP Gram stain and shape indicators:
Diplococci
Coccobacilli
Gram + diploccoci = S. pneumo
Gram - diplococci = N. meningitis
Gram + rod/coccobacilli = Listeria
Gram - coccobacilli = H-flu
Empiric Therapy for Meningitis
S.pneumo/Meningococcal = Cefotaxime or Ceftriaxone + Vancomycin
Listeria = Ampicillin + Gentamycin (TMP-SMX or Meropenem as PCN alternatives)
Nosocomial = Ceftazidime + Vancomycin
Brain Abscess Treatment: Otogenic or No obvious source
Otogenic: Cefotaxime 2g q8hr
No obvious source: Cefotaxime + Flagyl 1 g then 500mg q6hrs
Brain Abscess Treatment: Sinogenic/Odontogenic or Hematogenous
PCN 24 mill units/d divided q4hrs + Flagyl 1g then 500 mg q6hr
Brain Abscess Treatment: Penetrating trauma or neurosurgery
Nafcillin 2g q4h + Ceftazidime 2g q8h
CNS Neoplasm Classifications
Based on cellular origin and histologic appearance
Grade 1: benign
Grade 2: malignant
Grade 3: actively growing, malignant tissue
Grade 4: Grows quickly; cells look very abnormal; malignant
Schwannoma
Cranial and paraspinal nerve tumor of Schwann cell
Slow growing
Acoustic neuroma most common
-Unilateral hearing loss, tinnitus, and HA are key signs
Primary CNS Lymphoma
In immunodeficient pts
Derived from B lymphocytes, often in cerebral hemispheres
Tx: Once Dx is confirmed, Steroids to reduce edema and shrink tumor
Followed by chemo and radiation - usually too deep to operate
