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On Call Neurology > Neuro investigations > Flashcards

Neuro investigations Flashcards

1
Q

What are the indications for lumbar puncture?

A

Absolute:

  • meningitis
  • subarachnoid hemorrhage*

Relative:

  • peripheral neuropathy
  • carcinomatous meningitis
  • pseudomotor cerebri
  • multiple sclerosis (MS)
  • +++ inflammatory disorders

*if not diagnosed on CT head

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2
Q

What is another name for pseudomotor cerebri?

What is the definition of this?

Symptoms?

A
  • idiopathic intracranial hypertension
  • ↑ cerebrospinal fluid pressure in the brain
  • Because this condition causes symptoms of elevated pressure in the head – which is also seen with large brain tumors – but have normal scans, the condition has been called pseudotumor cerebri, meaning “false brain tumor”.

SYMPTOMS:

  • headache
  • blurred vision –> worse over time –> need early treatment may lead to progressive (and possibly permanent) loss of vision
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3
Q

Lumbar puncture protocol?

A

step 1: back at edge of bed, head flexed and legs curled up = fetal position

step 2: shoulders + hips are parallel and perpendicular to bed

step 3: find interspace between L4 and L5 which is between line connecting iliac crests

step 4: insert needle one level above (b/w L3 and L4)

step 5: sterilize area, inject 2% lidocaine, insert 20/22 gauge needle slightly headwards

step 6: “POP” when enter subarachnoid space

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4
Q

What are the basic tests on CSF?

A 
Opening pressure 
Cell count (2 cc) 
Protein and glucose (2 cc) 
gram stain and culture (2 cc) 
CSF VDRL (1 cc)
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5
Q

How is a CSF bleed vs. traumatic tap differentiated?

A

Xanthochromia!

yellowish tinge which is seen in REAL SAH (>12 hours old)

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6
Q

Common side effect of LP?

A

spinal headache!

continuous leak of CSF –> low ICP –> traction on dura (=pain sensitive)

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7
Q

Rare side effects of LP?

A

1) epidural hematoma
2) meningitis
3) tentorial herniation (if SOL or basilar meningitis)
4) complete spinal block

**these are relative contraindications, benefits vs. risks needed

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8
Q

What is darkest, lightest and medium on CT?

A

dark - air > fat

medium - normal brain

light - bone, metal > acute hemorrhage > subacute hemorrhage (3-14 days)

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9
Q

CTP uses and product?

A
  • IV contrast
  • color coded maps of cerebral blood flow, volume, mean transit time
  • use: hypoperfused brain area w/ stroke or SAH
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10
Q

CT angiography uses and product?

A
  • IV contrast
  • 3D images for cervical and large proximal intracranial arteries
  • use: extracranial carotid stenosis, proximal intracranial stenoses/occlusions, saccular intracranial aneurysms
  • limit: not that good for smaller vasculature
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11
Q

What is contraindication to MRI?

A

ferromagnetic objects (pacemaker, orthopedic pins, aneurysm clips)

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12
Q

T1 images - use, appearance?

A

use: anatomy

appearance:
- black = CSF, bone
- white = fat, subacute blood (>48 hours)

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13
Q

T2 images - use, appearance?

A

use: pathology (e.g. infarct, tumor)

appearance:
- white = water

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14
Q

What is FLAIR imaging?

A

Flair sequence is similar to a T2-weighted image except that the TE and TR times are very long.

By doing so, abnormalities remain bright but normal CSF fluid is attenuated and made dark.

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15
Q

What is diffusion weighted imaging? Uses?

A

Use = detecting hyperacute ischemia

*lesions on DWI become high intensity lesions on T2 and FLAIR

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16
Q

What are apparent diffusions coefficient maps?

A
  • compared with DWI, ADC maps are a purer image of restricted diffusion caused by ischemia and cytotoxic edema
  • restricted diffusion caused by ischemia appears black/dark on ADC
  • bright region = vasogenic edema
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17
Q

What are proton density images?

A

periventricular pathology (e.g. white matter demyelination) from CSF

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18
Q

What are STIR sequences?

A

Short tau inversion recovery sequences

SUM of T1 and T2 signals
SUBSTRACT fat

use: mesial temporal sclerosis in patients with epilepsy

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19
Q

What are flow voids?

A
  • look black on both T1 and T2

- high velocity blood flow (e.g. normal cerebral vessels or AVM)

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20
Q

MRA vs. MRV?

A

Magnetic resonance angiography:

  • blood vessels inside and outside the brain
  • SUBSTRACT brain and skull

Magnetic resonance venography:
- substraction images of major venous sinuses

21
Q

What is myelography?

A
  • Injecting radiopaque dye into spinal canal via lumbar or suboccipital approach
  • XR and CT show subarachnoid space and show extradural compressive lesions, ruptured intervertebral disks and vascular malformations on surface of cord
  • now replaced by MRI
22
Q

What is a carotid duplex doppler ultrasound used for?

A

use: noninvasive and accurate estimate of stenosis in extracranial internal carotid arteries
degree: (1) normal, (2) <40% stenosis, (3) 40% to 60% stenosis, (4) 60% to 80% stenosis, (5) 80% to 99% stenosis, and (6) occlusion

23
Q

If carotid ultrasound shows occlusions, what are the next steps?

A

angiography!

24
Q

Transcranial Doppler (TCD) ultrasonography is used for?

A

measuring the velocity of blood flow in the intracranial proximal cerebral arteries (ICA siphon, middle cerebral artery [MCA], anterior cerebral artery [ACA], posterior cerebral artery [PCA], ophthalmic, basilar, and vertebral)

25
Q

What is transcranial ultrasonography used for?

A
  • stenosis or occlusion in the cranium
  • hemodynamic significance of carotid stenosis or occlusions
  • vasospasm in patients with SAH
  • AVM screen ( look for high flow, low pulsatility)
  • ↑↑ ICP (low velocity flow, high pulsatility)
  • diagnosing brain death
26
Q

What is angiography? What is it used for?

A
  • done by threading small catheter into cerebral vessels in the femoral artery

Uses:

  • occluded or stenotic vessels
  • arterial dissections
  • aneurysms
  • AVMs
  • vasculitic narrowing (“beading”)
  • dural venous sinus thrombosis
27
Q

What are the complications of angiography?

A
  • infection at puncture site
  • bleeding at puncture site
  • stroke (1-2%) 2/2 catheter emboli with atherosclerotic disease
28
Q

Electromyography (EMG) procedure?

A

a needle electrode is inserted into a muscle and motor unit potentials are collected

  • at rest (spontaneous activity)
  • varying degrees of muscle contraction
29
Q

What are the EMG parameters and what do they tell you?

A
  • tells you neuropathic vs. myopathic disease
  • tells you exact distribution of muscle disorders with unique features (e.g. myotonia)

1) insertional activity
- -> nonspecific

2) spontaneous activity
- -> normal is silent
- -> contraction (fibrillation and positive sharp waves) + motor unit discharges (fasciculations) = denervation
- —> acute injury ==> spontaneous activity takes ~2 weeks to appear

3) motor unit potential
- -> neuropathic = reinnervation of previously denervated motor units = high amplitude, polyphasic potentials
- -> myopathic = muscle fiber mass loss = low amplitude, polyphasic potentials

4) recruitment pattern
- -> voluntary muscle contraction causes progressive recruitment of motor units and obliteration of baseline signals
- -> neuropathic disease fewer motor units in affected muscle causes reduced or discrete recruitment of motor units
- -> myopathic disease = random loss of muscle fibers (leads to early recruitment and low amplitude interference pattern)

5) single fibre EMG
- shows relationship of firing single muscle fibers innervated by same motor neuron
- impaired NM transmission causes varying interval = jitter

30
Q

Nerve conduction studies parameters?

A
  1. Conduction velocity.
    - demyelinating neuropathy = this is generally reduced (<60% of normal)
    - Conduction block = reflects focal demyelination and is identified when nerve
    stimulation proximal to the block leads to a compound muscle action potential (CMAP) amplitude that is less than 50%
    of that obtained by stimulating distal to the block.
  2. Amplitude.
    - The amplitude of the CMAP correlates with the
    number of muscle fibres activated by stimulation of the
    peripheral nerve. I
    - In general, reduced CMAP amplitude with
    relatively preserved conduction velocity is characteristic of
    axonal neuropathy.
  3. Late responses.
    - F waves result from antidromic conduction followed by orthodromic conduction in the same nerve.
    - Delayed or absent F waves, in combination with normal
    peripheral nerve conduction, implies disease of the proximal
    nerve (e.g., root compression, early Guillain-Barre syndrome).
    - The H reflex is the electrical counterpart of the ankle jerk and can be performed to assess the integrity of the S1 root; the antidromic potential travels down a sensory nerve, synapses in the spinal cord, and then travels orthodromically down a motor nerve.
  4. Repetitive stimulation.
    - Muscle responses to repetitive stimulation are useful for assessing neuromuscular junction disease.
    - In myasthenia gravis repetitive
    stimulation at 2 to 3 Hz produces a characteristic decremental response (>10% drop in amplitude between the first and the fifth CMAP).
31
Q

Nerve conduction studies procedure?

A
  • applying electrical
    stimulation to skin sites overlying a peripheral nerve
  • recording the speed of conduction and amplitude of the “downstream” action potential.
32
Q

Muscle and nerve biopsy

A

extremely fragile
procedure only by an experienced surgeon

The sural nerve and gastrocnemius muscle are often examined together, although biopsy of almost any muscle can be performed.

Muscle biopsy is essential for diagnosing causes of myopathy such as polymyositis, genetic biochemical deficiencies, mitochondrial disease, sarcoidosis, critical illness myopathy, and infection (e.g.,
trichinosis).

The causes of neuropathy that can be diagnosed by
nerve biopsy are listed in Table 20.4.

33
Q

Brain biopsy procedure?

A 
open procedure (usually
of the anterior nondominant temporal lobe) or by using stereotactic needle localization

Although stereotactic biopsy is often necessary for deep lesions, the diagnostic yield is better with the open procedure because more tissue can be obtained.

diagnostic yield maximized when areas of enhancement or signal abnormality on MR are targeted.

34
Q

Brain biopsy uses?

A 
brain tumors or abscess
central nervous system (CNS) vasculitis
neurosarcoidosis
viral encephalitis
heritable metabolic disorders
Jakob-Creutzfeldt disease
35
Q

Brain biopsy risks?

A

hemorrhage (in approximately 1% of cases)

36
Q

What are evoked potentials?

A

recording of electrical activity in central sensory pathways produced by visual, auditory, or sensory stimulation.

Signals are recorded by placing electrodes over the
scalp or the spine and using a computer to average and amplify the signal, which results in a characteristic pattern of waveform peaks that have approximate anatomic correlates

37
Q

What are 3 types of evoked potential studies?

A
  • Visual evoked responses (VERs)
  • Brain stem auditory evoked responses (BAERs)
  • Somatosensory evoked potentials (SSEPs)
38
Q

Visual evoked responses (VERs)

A

visual stimulus is delivered as an alternating checkerboard
pattern or a stroboscopic flash

the waveform corresponds
with stimulation of the occipital cortex

39
Q

Brain stem auditory evoked responses (BAERs)

A

Auditory signals are delivered by clicks through earphones.

The waveform corresponds with stimulation of CN 8, the
cochlear nucleus, pons, and inferior colliculus

40
Q

Somatosensory evoked potentials (SSEPs)

A

Electrical stimuli are delivered to peripheral nerves.

waveform corresponds with stimulation of the lumbosacral
or the brachial plexus, the cervicomedullary dorsal column
nuclei, and the sensory cortex (the N20 potential).

41
Q

What are the uses of evoked potentials?

A
  1. Multiple sclerosis. Evoked potentials can be used to support the diagnosis in a patient with a single symptom by identifying subclinical demyelination at a different anatomic site (e.g., abnormal VERs in a patient with transverse myelitis).
  2. Brain stem lesions. These can be verified and localized
    with BAER.
  3. Acoustic neuroma. BAER can be used to verify CN 8 injury.
  4. Spinal cord injury. SSEP can be used for prognosis by differentiating complete from partial injury.
  5. Hypoxic-ischemic coma. Bilateral absence of the N20 cortical potentials by SSEP on day 5 or later implies with a high degree of certainty that consciousness will not be regained.
42
Q

Electroencephalography procedure? Usual diagnosis?

A
  • electrodes on the brain collect surface electrical activity
  • rhythms are analyzed to come up with diagnosis

usually looking for epilepsy activiy

43
Q

Normal EEG

A

awake:
- posterior dominant alpha rhythm

sleep:
- progressive slowing –> vertex transients –> sleep spindles –> K complexes

44
Q

Uses of continuous EEG

A
  • ICU where patient has known non-convulsive status epilepticus
  • general w/u coma patient to find non-clinical seizure (10-30%)
45
Q

Is EEG always going to pick up on seizure activity?

A

NO!

20-40% recordings patients epilepsy look normal

46
Q

What are activation procedures?

A

In seizure context, they are actions with elicit epileptiform activity or absence seizures

Procedures:

  • sleep
  • sleep deprivation
  • hyperventilation
  • photostimulation
47
Q

What does a seizure typically look like on EEG?

A
  • distinct onset, evolution and offset of rhythmic spikes
  • sharp waves
  • ictal-appearing discharges
  • lasting at least 10 seconds
48
Q

What is needed to confirm a non-convulsive status epilepticus in patient with prolonged post-ictal or impaired consciousness?

A

CONTINUOUS EEG

49
Q

What are types of non-convulsive status epilepticus?

A

complex partial seizure

absence seizure

On Call Neurology (4 decks)

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