Neurology Shelf

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Neurology Shelf
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  1. CSF Background
    -production
    -movement
    -total volume
    • -produced by choroid plexus
    • -absorbed through arachnoid granulations

    Rate of production = 0.5 mL/min

    Total volume = 150 mL

  2. CSF Glucose
    Normal = 2/3 of blood glucose

    • Decreased in:
    • -bacterial
    • -mycobacterial infection
  3. CSF Protein
    Normal = 15-45 mg/dL

    • Increased in:
    • -Infection (fungal, mycobacterial)
    • -Demyelination
    • -Tumor
    • -Sarcoidosis
    • -Age
  4. CSF WBCs
    Normal < 5 cells

    • Polys:
    • -bacterial infection
    • -early viral infection

    • Lymphs:
    • -viral infection
    • -fungal infection
    • -mycobacterial infection
    • -demyelination (MS, ADEM)
    • -CNS lymphoma
  5. CSF Opening Pressure
    Normal: 60-150 mmHg water
  6. Lumbar Puncture
    -Procedure
    -Contraindications
    -Complications
    • Procedure:
    • -laterally recumbant with knees up
    • -L3-L4 (palpate across from ASIS)
    • -insert bevel upwards, slightly rostral
    • -CT before except if suspect bacterial meningitis

    • Contraindications:
    • -supratentorial, infratentorial mass
    • -closure of 4th ventricle

    • Complications
    • -Low pressure HA (lie down, liquids, caffeine, epidural blood patch)
  7. Common Disease CSF Findings
  8. CT Imaging
    -background
    -use
    -adverse effects
    • Background:
    • -xrays

    • Initial Imaging for:
    • -HA
    • -Trauma
    • -Seizures
    • -Subarachnoid hemorrhage
    • -Stroke

    • Contrast:
    • -iodinated
    • -nephrotoxic
    • -shows disruption in BBB

    • Adverse Effects:
    • -contraindicated in pregnancy
    • -contrast is nephrotoxic

    • White:
    • -bone
    • -acute blood (dark after 3 weeks)
    • -calcification
  9. MRI Imaging
    -background
    -TE
    -TR
    -Contrast
    -Types
    • Background:
    • -radiofrequency pulses (excite hydrogen ions)

    • Time to Echo (TE):
    • -time interval before signal intensity is measured

    • Time to Repetition (TR):
    • -time between RF pulses

    • Contrast:
    • -gadolinium
    • -not nephrotoxic
    • -usually use T1
    • -show breakdown in BBB
    • -brain tumors, abscesses, inflammation, new MS lesions

    • Types:
    • -T1
    • -T2
    • -FLAIR
    • -SWI
    • -DWI

    • Use:
    • -better anatomic definition
    • -contents of posterior fossa
    • -contents of craniocervical junction
    • -DWI in early stroke

    • Complications:
    • -can't use in patients with metal objects
    • -claustrophobia
  10. T1 MRI
    -short TE and TR

    • Bright:
    • -fat
    • -white matter (myelin)

    • Dark:
    • -water (CSF)

  11. T2 MRI
    -long TE and TR

    • Bright:
    • -water (CSF)

    *use to evaluate spinal cord

  12. FLAIR MRI
    -background
    -use
    "Fluid-attenuated Inversion Recovery"

    • Background:
    • -strong T2 weighted --> CSF signal inverted (dark)

    • Use:
    • -best imaging for most pathologic processes
    • -best imaging for chronic MS lesions

  13. SWI MRI
    "Susceptibility-weighted Images"

    • Background:
    • -sensitive to disruption of substance on magnetic field
    • -Substances = Calcium, bone, blood breakdown products (ferritin, hemosiderin)
    • -appear black
  14. DWI MRI
    "Diffusion-weighted Images"

    • Background:
    • -demonstrates cellular toxicity with high sensitivity

    • Use:
    • -diagnosis of acute stroke (may be positive 30 min after onset)

    • Bright:
    • -areas of restricted diffusion

  15. Conventional Angiography
    -procedure
    -pros
    -cons
    • Procedure:
    • -cannulation of great vessels with injection of contrast dye

    • Pros:
    • -most sensitive and specific

    • Cons:
    • -contrast dye reaction
    • -stroke due to plaque dislodged by catheter
    • -bleeding from cannulation site
  16. MRA
    -procedure
    -pros
    -cons
    -use
    Magnetic Resonance Angiography

    • Procedure:
    • -uses blood flow as a contrast agent

    • Pros:
    • -less invasive
    • -quick

    • Cons:
    • -less sensitive and specific

    • Use:
    • -stroke patients (vascular narrowing/occlusion)
    • -vertebral/carotid artery dissection ("fat-suppressed MRA")
  17. MRV
    -use
    Magnetic Resonance Venography

    • Use:
    • -demonstrate venous sinus thrombosis and other venous diseases
  18. PET
    Positron Emission Tomography

    • Procedure:
    • -measures regional brain metabolism

    • Hypermetabolism:
    • -seizures

    • Hypometabolism:
    • -interictally (useful in planning epileptic surgery)
  19. SPECT
    Single-Photon Emission CT

    • Procedure:
    • -uses radioactive isotope to demonstrate increased blood flow during seizures
  20. EEG
    -procedure
    -bipolar montage
    -referential montage
    -alpha
    -beta
    -theta
    -delta
    Electroencephalography

    • Procedure:
    • -provides a record of electrical activity of cerebral cortex
    • -patterns correlate with degree of wakefulness or sleep
    • -sum of excitatory and inhibitory postsynaptic potentials of cortical neurons

    • Bipolar Montage:
    • -all electrodes are active
    • -read btwn adjacent electrodes

    • Referential Montage:
    • -read electrode activity beneath active electrode relative to distant electrode

    • ALPHA:
    • -8-13 Hz
    • -over posterior head in the relaxed awake state with the eyes closed

    • BETA:
    • ->13 Hz
    • -more prominent over frontal regions

    • THETA:
    • -4-7 Hz
    • -normal during drowsiness and sleep

    • DELTA:
    • -<4 Hz
    • -normal during drowsiness and sleep
  21. Clinical Utility of EEG
    • Limitations:
    • -patterns rarely specific to their cause
    • -may be insensitive to deep structures
    • -can be normal in ppl with paroxysmal disorders
  22. Nerve Conduction Studies
    1. MOTOR
    -CMAP
    -Distal Latency
    -Conduction Velocity
    2. SENSORY
    • 1. MOTOR STUDIES:
    • -electrodes over endplate of the muscle
    • -stimulate nerve

    • CMAP (Compound Muscle Action Potential):
    • -recording of contraction of underlying muscle

    • Distal Latency:
    • -time interval between stimulation over the distal portion of the nerve and the initiation of the CMAP

    • Conduction Velocity:
    • -difference in the latency to CMAP initiation between proximal and distal sites of stimulation

    • 2. SENSORY STUDIES:
    • -nerve stimulated at one site, record AP at more proximal site (orthodromic) or more distal site (antidromic)
  23. EMG
    -procedure
    -recruitment
    -activation
    -disease processes
    • Electromyography
    • -insertion of needle into individual muscles
    • -measure electrical activity on insertion, at rest and during contraction

    Recruitment = more motor units being added

    Activation = motor units fire more quickly

    • Reduced Recruitment:
    • -LMN disease

    • Early Recruitment:
    • -myopathic disease
  24. EMG in Neurogenic Disorders
    -insertional activity
    -spontaneous activity
    -VMUP
    -Recruitment
    • Insertional Activity:
    • -increased (active denervation)

    • Spontaneous Activity:
    • -increased (active denervation)

    • Volitional Motor Unit Potentials:
    • -Large amplitude
    • -polyphasic

    • Recruitment:
    • -reduced
  25. EMG in Myopathic Disorders
    -insertional activity
    -spontaneous activity
    -VMUP
    -Recruitment
    • Insertional Activity:
    • -Usually normal

    • Spontaneous Activity:
    • -usually normal

    • Volitional Motor Unit Potentials:
    • -small amplitude
    • -polyphasic

    • Recruitment:
    • -usually normal early
  26. NCS in Demyelinating Neuropathies
    -Distal Latency
    -Conduction Velocity
    -CMAP Amplitude
    • Distal Latency:
    • -markedly prolonged

    • Conduction Velocity:
    • -markedly reduced

    • CMAP Amplitude:
    • -Normal or mildly reduced
  27. NCS in Axonal Neuropathies
    -Distal Latency
    -Conduction Velocity
    -CMAP Amplitude
    • Distal Latency:
    • -normal

    • Conduction Velocity:
    • -normal

    • CMAP Amplitude:
    • -Reduced
  28. Coma
    -state of unarousable unresponsiveness

    -alterations short of coma = drowsiness, lethargy, obtundation, stupor
  29. Clinical Approach to Coma
    1. ABCs

    • 2. Look for obvious clues to etiology
    • -hx of medical problems
    • -brief hx/general exam
    • -meningeal signs

    • 3. Try reversing common etiologies
    • -Naloxone
    • -Thaimine (always before glucose)
    • -Dextrose

    4. Check Brain stem reflexes and look for focal signs
  30. Coma: Mental Status Examination
    • -loud voice
    • -sternal rub
  31. Coma: Cranial Nerves Examination
    Assess brainstem function!

    • If can't arouse test brainstem reflexes
    • -Pupillary
    • -Corneal
    • -Oculocephalic
    • -Gag

    Fundoscopic Exam

    Blink to visual threat (test visual fields)
  32. Brainstem Reflexes
  33. Coma: Motor Tone Examination
    Extend limbs and hold (observe for downward drift)

    Check for movement in response to noxious stimuli

    Decorticate and decerebrate posturing
  34. Decorticate


    • -"to the core"
    • -brainstem dysfunction
    • -more superior lesion than decerebrate
  35. Decerebrate
  36. Coma: Muscle Stretch Reflex Examination
    • -Babinski sign
    • -normal reflex testing
  37. Coma: Sensory, Coordination, Gait
    -if patient is arousable enough
  38. Coma: two main causes
    • 1. Brainstem Dysfunction
    • -presence or absence of brainstem reflexes suggest how deep the coma is

    • 2. Simultaneous bilateral cerebral hemisphere dysfunction
    • -focal signs present --> structural cause
    • -focal signs absent --> diffuse cause

    (3. Mass effect)
  39. Coma: Focal Signs
    -examples
    • Examples:
    • -hemiparesis
    • -aphasia
    • -reflex asymmetry
    • -facial droop
    • -unilateral babinski
  40. Structural Causes of Depressed Consciousness
    1. Acute ischemic stroke

    2. Acute intracranial hemorrhage

    3. Brain tumor (with edema and hemorrhage)

    4. Brain abscess
  41. Diffuse Causes of Depressed Consciousness
    • METABOLIC
    • 1. Electrolyte Abnormality
    •      -hypo/hyper-natremia
    •      -hypo/hyper-calcemia
    •      -hypo/hyper-magnesemia
    •      -hypophosphatemia
    • 2. Glucose Abnormality
    •      -hypoglycemia
    •      -nonketotic hyperosmolar coma
    •      -DKA
    • 3. Hepatic failure
    • 4. Uremia
    • 5. Thyroid dysfunction
    •      -myxedema coma
    •      -thyrotoxicosis
    • 6. Adrenal Insufficiency

    • TOXIC
    • -Alcohol
    • -Sedatives
    • -Narcotics
    • -Psychotropic Drugs
    • -Exogenous toxins (CO, heavy metals)

    • INFECTIOUS:
    • -Meningitis
    • -Diffuse encephalitis

    • HYPOXIC-ISCHEMIC:
    • -respiratory failure
    • -cardiac arrest

    • OTHER:
    • -Subarachnoid hemorrhage
    • -Carcinomatous meningitis
    • -seizures or postical state
  42. Coma: Lab and Radiographic Studies
    • If suspect structural:
    • -urgent imaging (noncontrast CT)

    • If suspect diffuse:
    • -metabolic, toxic or infectious cause workup
    • -head imaging (cerebral edema, global hypoxic-ischemic injury, bilateral injury)

    Head CT before LP

    • EEG:
    • -can assess the depth of coma
    • -occasionally suggest specific diagnosis
  43. Coma: prognosis
    • Varies widely depending on:
    • -etiology
    • -age
    • -duration of cardiopulmonary arrest
  44. Persistent Vegetative State
    -loss of all awareness and cognitive function

    -may remain awake with eyes open, exhibit sleep-wake cycles, maintain respiration and other autonomic function

    -patients may progress to this state if they have been in a coma for a prolonged period
  45. Locked-In Syndrome
    • Presentation:
    • -patient is awake and may be intact cognitively
    • -unable to move extremities and most of face
    • -present vertical eye movements or blinks

    • Cause:
    • -usually large lesions in base of pons
  46. Brain Death
    • -irreversible cessation of all functions of the entire brain including the brainstem
    • -patient must be comatose, have absent brainstem reflexes

    • Tests:
    • 1. Apnea Test: no respirations even when CO2 allowed to rise
    • 2. EEG ("flat line")
    • 3. Cerebral angiography (absence of blood flow)
  47. Acute Confusional State
    -definition
    -DDx
    -causes
    • Definition:
    • "confusion", "delerium", "encephalopathy"
    • -problem of attention

    • DDx:
    • -aphasia (particularly Wernicke)
    • -psychosis
    • -complex partial seizures

    • Causes:
    • -infection
    • -metabolic disturbance
    • -inflammatory condition
    • -hypoxic-ischemic state
    • -focal brain disorders (particularly R hemisphere lesions)
  48. Neuromuscular Junction Disorders
    -pattern of weakness
    -associated sxs
    -lab studies
    -DDx
    • Pattern of Weakness:
    • -mostly affect proximal muscles
    • -fluctuation of weakness (can vary from hour to hour)
    • -fatigability

    • Associated Sxs:
    • -NO sensory sxs
    • -may have associated autonomic sxs

    • Lab Studies:
    • -EMG/NCS
    • -serum findings (antibodies)

    • DDx:
    • -Myasthenia gravis
    • -Lambert-Eaton Syndrome
    • -Muscular Dystrophy (Duchenne's, Becker)
    • -Myotonic Dystrophy
    • -Emery-Dreifuss Muscular Dystrophy
    • -Channelopathies
    • -Mitochondrial Myopathies
    • -Polymyositis
    • -Dermatomyositis
    • -Inclusion Body Myositis
    • -Neuroleptic Malignant Syndrome
  49. Peripheral Nerve Disorders
    -pattern of weakness
    -associated sxs
    -lab studies
    -DDx
    • Pattern of Weakness:
    • -specific muscle, not neighboring
    • -mononeuropathy multiplex (multiple nerves in succession)
    • -polyneuropathy (usually distal muscles first)

    • Associated Sxs:
    • -mononeuropathies: may have sensory problems (numbness, tingling, pain)
    • -Polyneuropathies: usually have sensory loss, and depressed/absent reflexes

    • Lab Studies:
    • -EMG: acuity vs chronicity
    • -NCS: axon vs myelin

    • DDx:
    • -Guillain Barre Syndrome
    • -Chronic Inflammatory Demyelinating Polyneuropathy
    • -Multifocal Motor Neuropathy
    • -Neuropathies associated with MM
    • -Diabetic Polyneuropathy
    • -Metabolic Neuropathies
    • -Hereditary Neuropathies
    • -Infectious Neuropathies
    • -Entrapment Neuropathies
    • -Autonomic Neuropathies
  50. Nerve Root Disorders
    -pattern of weakness
    -associated sxs
    -lab studies
    -DDx
    • Pattern of Weakness:
    • -radiculopathy
    • -muscles innervated by nerve root affected, not neighboring muscles

    • Associated Sxs:
    • -tingling or pain (radiating out of neck or back)
    • -reflex may be diminished
    • -rarely have sensory loss

    • Lab Studies:
    • -EMG/NCS: distinguish radiculopathy from polyneuropathy
    • -MRI spine
    • -LP: Polyradiculopathy

    • DDx:
    • -herniated discs
    • -shingles
    • -inflammatory/infectious (polyradiculopathy)
  51. Plexus Disorders
    -pattern of weakness
    -associated sxs
    -lab studies
    -DDx
    • Pattern of Weakness:
    • -multiple muscles in a limb are weak and don't follow pattern of particular nerve root or peripheral nerve

    • Associated sxs:
    • -associated sensory findings
    • -dropped reflexes

    • Lab Studies:
    • -EMG/NCS: confirm localization to plexus
    • -MRI: rule out mass lesions

    • DDx:
    • -inflammation
    • -radiation
    • -mets
    • -hemorrhage
    • -trauma
    • -diabetic amyoptrophy (lumbosacral plexopathy)
  52. Spinal Cord Disorders
    -pattern of weakness
    -associated sxs
    -lab studies
    -DDx
    • Pattern of Weakness
    • -anterior horn cells: weakness of muscles innervated by nerve root at that level (mimics radiculopathy)
    • -corticospinal tract: weakness below level of lesion (UMN pattern)

    • Associated Sxs:
    • -may be sensory findings
    • -reflexes increased below lesion
    • -Babinski sign
    • -bladder/bowel incontinence

    • Lab Studies:
    • -MRI spine
    • -LP

    • DDx:
    • -transverse myelitis (inflammation)
    • -infarction
    • -compression
    • -ALS
  53. Disorders of Cerebral Hemispheres and Brainstem
    -pattern of weakness
    -associated sxs
    -lab studies
    -DDx
    • Pattern of Weakness:
    • -weakness of contralateral body in UMN pattern
    • -homunculus
    • -lesions at base of pons (crossed signs: weakness of ipsilateral face and contralateral body)

    • Associated Sxs:
    • -cognitive signs
    • -L hemisphere: aphasia
    • -R hemisphere: neglect/visuospatial dysfunction
    • -Brainstem: CN problems

    • Lab Studies:
    • -MRI/CT

    • DDx:
    • -stroke
    • -demyelinating disease
    • -traumatic injury
    • -brain tumor
    • -infection
  54. Paresthesias
    "pins and needles"
  55. Dysesthesias
    -unpleasant sensations triggered by painless stimuli
  56. Hyperesthesia
    -increased sensitivity to sensory stimuli
  57. Allodynia
    -pain provoked by normally innocuous stimuli
  58. Dissociated sensory loss
    -loss of one of the sensory systems with preservation of another

    EG: syrinx (STT compromised first)
  59. Approach to the patient with Vertigo
    1. Spontaneous
         a) single prolonged episode
         b) recurrent episodes
    2. Positional
         a) peripheral
         b) central
    • 1. SPONTANEOUS VERTIGO
    •      a) Single Prolonged Episode
    •           -vestibular neuronitis
    •           -labyrinthine concussion
    •           -lateral medullar/cerebellar infarction
    •      b) Recurrent Episodes
    •           -Meniere Disease
    •           -Perilymph fistula
    •           -Migraine
    •           -Posterior circulation ischemia

    • 2. POSITIONAL VERTIGO
    •      a) Peripheral
    •           -BPPV
    •      b) Central
  60. Signs of Peripheral vs Central Vertigo
    • Peripheral:
    • -tinnitus
    • -hearing loss

    • Central:
    • -diplopia
    • -dysarthria
    • -dysphagia
    • -brainstem dysfunction
    • -vertical nystagmus
    • -direction-changing gaze-evoked nystagmus
  61. Vestibular Neuronitis
    -presentation
    -pathophysiology
    -course
    • Presentation:
    • -acute
    • -unilateral
    • -nausea/vomiting

    • Pathophysiology:
    • -no evidence of inflammation

    • Course:
    • -sx peak withing 24 hours
    • -improve over days to weeks
    • -recovery due to central compensation
  62. Labyrinthine Concussion
    -etiology
    -presentation
    • Etiology:
    • -head injury (even w/o skull fracture)

    • Presentation:
    • -vertigo
    • -sometimes hearing loss/tinnitus
  63. Infarction of labyrinth, brainstem, cerebellum
    -blood supply
    -presentation of infarct
    • Blood supply to central/peripheral vestibular apparatus, cerebellum:
    • -vertebrobasilar system
    • -PICA
    • -AICA
    • -superior cerebellar artery

    • Blood supply to inner ear:
    • -internal auditory artery (of AICA)

    • Presentation internal ear infarct:
    • -sudden onset deafness, vertigo or both

    • Presentation of brainstem/cerebellar stroke:
    • -central-type nystagmus
    • -associated CN signs
    • -weakness
    • -ataxia
    • -sensory changes
  64. Meniere Disease
    -presentation
    -pathophysiology
    • Presentation:
    • -nausea/vomiting
    • -fluctuating but progressive hearing loss
    • -tinnitus
    • -sensation of aural fullness

    • Pathophysiology:
    • -intermittent increase in endolymphatic volume
  65. Perilymph Fistula
    -presentation
    • Presentation:
    • -pt hears a "pop" at a time of sudden increase in middle ear pressure
    • -abrupt onset of vertigo
  66. BPPV
    -presentation
    -pathophysiology
    -diagnosis
    -treatment
    • Presentation:
    • -episodes of vertigo precipitated by changes in position
    • -seconds to minutes
    • -few seconds latency
    • -associated severe n/v
    • -may occur in clusters

    • Pathophysiology:
    • -loose otoliths in SCC

    • Diagnosis:
    • -downbeating and torsional nystagmus with Dix-Hallpike test
    • -offending ear to the ground when vertigo occurs

    • Treatment:
    • -Epley manuever
  67. Causes of Syncope

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