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Neuroanatomy/Pathology- Berkowitz Flashcards

1
Q

Examination of mental status includes:

A
  1. Level of consciousness
  2. Integrity of individual cognitive functions (attention, memory, language, calculation, abstract reasoning, praxis)
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2
Q

What areas of brain control consciousness?

A

RAS, thalami, & cerebral hemispheres

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3
Q

What is delirium?

A

Fluctuating acute confusion

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4
Q

What is lethargy/somnolence?

A

Falling asleep without repetitive stimulation

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5
Q

What is being stuporous?

A

Requiring painful and/or painful physical stimulation to be awakened

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6
Q

What is obtundation?

A

Between somnolent & stuporous

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7
Q

What domain of cognitive assessment should be done first, because if not in tact, the rest cannot be tested?

A

Attention

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8
Q

What lobes control attention?

A

Frontal & parietal

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9
Q

Examples of testing attention

A
  1. Digit span- recite a string of #’s backward & forwards
  2. Months backwards
  3. Spell “world” backwards
  4. Serial 7’s
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10
Q

What is a core feature of delirium?

A

Inattention

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11
Q

Where is the lesion if someone neglects one half of the world?

A

Parietal (most commonly right parietal lesions causing left hemi-neglect)

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12
Q

What lobe provides ability for memory?

A

Temporal lobe

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13
Q

Even with profound memory loss, people should remember their name. If they cannot, it is usually:

A

Psychiatric

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14
Q

Testing short term memory

A

Give 3 words to recite & remember & ask them to repeat 5 minutes later

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15
Q

Why does amnesia usually occur?

A

Damage to one or both temporal lobes, specifically medial temporal lobe- hippocampus

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16
Q

Deficits in memory are core features of:

A
  1. Alzheimer’s
  2. Transient global amnesia
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17
Q

What lobes provide language?

A

Frontal & temporal lobes (most commonly in left hemisphere)

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18
Q

What hemisphere usually controls language?

A

Left (for all right-handed people & most left-handed people)

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19
Q

Where is Broca’s area?

A

Left inferior frontal gyrus

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20
Q

Where is Wernicke’s area?

A

Left posterior superior temporal gyrus

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21
Q

Bedside tests that test cognitive function across multiple domains

A
  1. MMSE (mini-mental state examination)
  2. MoCA (Montreal cognitive assessment)
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22
Q

Cranial Nerves

A

1: Olfactory
2: Optic
3: Oculomotor
4: Trochlear
5: Trigeminal
6: Abducens
7: Facial
8: Vestibulocochlear
9: Glossophrangeal
10: Vagus
11: Spinal Accessory
12: Hypoglossal

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23
Q

Olfactory nerve

A

Smell from nose to olfactory cortex (inferior frontal & medial temporal lobes)

Only CN that sends signal directly to cortex without stopping at thalamus (although olfactory cortex does send projections to thalamus)

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24
Q

Optic nerve

A

Transmits visual info from retina to occipital cortex

Also transmits light info to midbrain as afferent limb of pupillary light reflex

Only nerve that can be visualized on exam (fundoscopy)

Only CN that is part of the CNS; all the rest are PNS

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25
Q

Oculomotor, Trochlear, & Abducens nerves

A

Control movement of eyes

Oculomotor also controls elevation of eyelid & constriction of pupil

Examining ability to look in specific direction (saccades) & follow examiner’s finger (smooth pursuit) tests these 3 nerves, their interconnections, brainstem pathways, cerebellum, & cortical eye fields

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26
Q

Trigeminal nerve

A

Transmits facial sensation to sensory cortex via brainstem & ventral posterior medial nucleus of thalamus

Controls muscles of mastication

Facial sensation: VPM of thalamus to post-central gyrus

Motor: Pre-central gyrus to jaw musculature

Carries afferent limb of corneal reflex (efferent limb travels via facial nerve)

Provides both afferent & efferent limb of jaw jerk reflex

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27
Q

Facial nerve

A

Tested by asking patients to raise eyebrows & close eyes tightly (upper facial muscles); smile for lower facial muscles

28
Q

Vestibulocochlear nerve

A

Hearing: sound from exterior > inner ear > nerve > brainstem & thalamus > auditory cortex in superior temporal lobe

29
Q

Glossopharangeal & Vagus nerves

A

Innervate muscles of larynx & pharanx with afferent & efferent visceral autonomic functions

Dysfunction: dysarthria, hypophonia, and/or dysphagia

Assessed via palate elevation (primarily vagus) & gag reflex (afferent via glossopharangeal, efferent via vagus)

30
Q

Spinal accessory nerve

A

Controls trap & SCM

Along with CN 1, is the only other CN that does not make contact with brainstem

Comprised of spinal roots, but exits skull with other CN via jugular foramen

31
Q

Hypoglossal nerve

A

Controls muscles of tongue

Like facial nerve & motor component of trigeminal nerve, motor control comes from motor cortex at pre-central gyrus, so weakness of tongue on one side can localize anywhere along the pathway from contralateral motor cortex to its connections with CN12 nucleus in the medulla or even at CN12 itself

32
Q

Motor system

A

Brain > brainstem > spinal cord > ventral nerve roots > peripheral nerves > NMJ > muscle

33
Q

Paresis vs plegia

A

Paresis: weakness
Plegia: paralysis

34
Q

What is trigeminal neuralgia commonly caused by?

A

Compression via superior cerebellar artery pulsating directly on nerve

35
Q

Sensory exam

A

Begins in skin (vibration, temp, light touch, pain) & tendons/muscles (proprioception). Peripheral nerves carry information to spinal cord via dorsal root ganglia (DRG) & dorsal roots

Sensory info then travels through brainstem, thalamus, & finally somatosensory cortex in the anterior parietal lobe (post-central gyrus)

36
Q

Tested reflexes

A

Biceps: C5-6
Brachioradialis: C6
Triceps: C7-8
Patellar: L3-4
Ankle/achilles: S1-2

37
Q

If you need to elicit reflexes via Jendrassik maneuver or other type of assistance:

A

Hyporeflexia is present (or not relaxed)

38
Q

Sign of hyper-reflexia

A

Spread of reflex from one tested area to an adjacent area (eliciting biceps causes simultaneous finger flexion or eliciting patellar causes ankle plantarflexion)

39
Q

Pathologic reflexes

A

Babinski- normal response is flexion (down-going); abnormal is an extensor response (extension of big toe which may be accompanied by fanning of all toes or triple flexion- ankle dorsiflexion, knee flexion, hip flexion); a/w lesion of CNS at corticospinal tract

Chaddock sign- extension of big toe with stroking lateral aspect of dorsum of foot from lateral mal to 5th toe

Oppenheim sign- extension of big toe with stroking tibia downward to foot

Gordon sign- extension of big toe with squeeze of calf

Bing sign- extension of big toe with pinch of one of the toes (pricking dorsum of 4th or 5th toe)

Hoffman (flicking down), Traubner (flicking up) of middle finger- analagous to Babinski for UE

40
Q

Exams for coordination

A

Have patient move index finger back & forth between examiner’s finger & patient’s nose, sliding heel down shin, performing rapid alternating movements

When performing finger-to-nose, make sure patient’s arms get fully extended otherwise subtle ataxia at extremes of motion can get missed

41
Q

Ataxia

A

Uncoordinated movements

42
Q

Dysmetria

A

Inaccuracy of movements (under or overshooting target)

43
Q

Dysdiadochokinesia

A

Uncoordinated RAM

44
Q

Why does ataxia, dysmetria, or dysdiadochokinesia occur?

A

Disorder of cerebellum

Note the cerebellum needs proprioceptive input to perform coordination; ataxia can therefore also be caused by impaired proprioception via peripheral nerve, DRG, dorsal root, or spinal cord disease (sensory ataxia)

45
Q

Parkinsonian gait

A

Stooped, small-stepped, shuffling gait with difficulty turning

46
Q

Magnetic gait

A

Feet lifted briefly off the ground before being returned briskly to ground seen in NPH & with proprioception dysfunction

47
Q

Ataxic gait

A

Wide-based & unsteady gait seen in cerebellar dysfunction (like being drunk) & severe proprioception dysfunction

48
Q

Spastic gait

A

Leg extended, foot plantarflexed, entire leg circumducted with each step. If both legs are spastic –> scissoring. Seen with CNS dysfunction of motor system

49
Q

Does bacterial or viral/fungal infection abscess in brain appear more acutely clinically?

A

Bacterial; viral/fungal can take a few days to show itself

50
Q

Why is CT not great when evaluating posterior fossa?

A

Beam-hardening artifact

51
Q

Does MRI have radiation exposure?

A

No

52
Q

CT vs MRI

A

MRI takes longer, more expensive, cannot be performed in patients with ferromagnetic device in body, or exposure to shrapnel

53
Q

Can CT or MRI use different windows to highlight different portions of an image?

A

CT

54
Q

How does CT work?

A

Relies on different densities of tissues to generate image

Denser: hyperdense (bone)
Less dense: hypodense (air)

CSF is denser than air but not as dense as bone, & brain is denser than CSF

Gray matter is denser than white matter, so cortex & deep gray matter structures (BG & thalamus) are brighter than white matter

55
Q

Causes of hyperdensity on CT

A

Most common: hemorrhage & calcification (also contrast)

If unable to distinguish hemorrhage vs calcification from history, can use Hounsfield units-
60-100: blood
100-200: calcification (normal in choroid plexus, falx cerebri, pineal gland, & in some older people’s BG; abnormal in tumors or infectious lesions like neurocysticercosis)
>1000: bone

Other pathologic hyperdensities:
- Hyper-cellular tumor (lymphoma)
- Thrombosed blood vessel (hyperdense vessel sign in acute ischemic CVA & cord sign in venous sinus thrombosis)
- Atherosclerotic plaques in arteries
- Contrast-enhancing lesions: tumor, abscess, acute demyelination, subacute CVA

56
Q

Causes of hypodensity on CT

A

Any pathology that causes edema:
- Tumor
- Inflammation
- Infection
- Trauma
- Ischemic CVA (after acute phase)

Sequelae of prior injury (trauma, infarct, demyelinating lesion)

57
Q

Ischemic CVA vs other causes of hypodensity on CT

A

CVA respects a vascular territory so have clear, distinct borders

Edema around a tumor, infectious lesions, or acute demyelinating lesions have less distinct boundaries

If the hypodensity is near cortical surface, an infarct will most often include the cortex since a cortical vessel will supply both the cortex & underlying white matter. In contrast, most infectious, neoplastic, & demyelinating lesions involve the sub-cortical white matter so the hypodensity will usually respect the gray-white matter boundary, sparing overlying cortex

58
Q

MRI sequences to evaluate brain

A

T1, T2, FLAIR (fluid-attenuated inversion recovery, DWI & ADC (apparent diffusion coefficient), SWI (or GRE- gradient echo)- all are different in the way they are acquired

59
Q

T1-weighted images

A

Gray matter is darker than white matter

CSF is dark

60
Q

T2-weighted images

A

Appear as a “negative” of T1 images; white matter is darker than gray matter & CSF is bright

Most pathology shows up bright (hyperintense) on T2 & dark (hypointense) on T1

61
Q

FLAIR

A

T2-weighted sequence with suppression of bright CSF signal –> makes T2 hyperintense pathology more easily visible (good example is peri-ventricular lesions which is near a lot of CSF)

T2 hyperintensities are better seen in brainstem than would be on FLAIR, however

62
Q

General use for T1 vs T2/FLAIR

A

T1: examine brain structure

T2/FLAIR: looks for hyperintensities suggestive of pathology

When contrast is administered, post-contrast T1-weighted images are compared to pre-contrast to look for abnormal regions of enhancement

63
Q

Appearance of blood on MRI depending on age

A

T1:T2
Hyperacute- Isointense:Hyperintense
Acute- Isointense:Hypointense
Early subacute- Hyper:Hypo
Late subacute- Hyper:Hyper
Chronic- Hypo:Hypo

64
Q

DWI & ADC

A

Most commonly used in the evolution of acute ischemic CVA (seen within minutes)

Evaluate ease of water passing through tissues

Brain is much less defined on these images (scalp & soft tissue not visible)

Areas that diffuse water less easily –> diffusion restriction –> bright on DWI & dark on ADC

If bright on DWI, but not dark on ADC –> artifact or “T2 shine through” if also bright on T2/FLAIR

The cause of diffusion restriction in acute ischemic CVA is cytotoxic edema

Diffusion restriction can also be seen in Creutzfeldt-Jakob (in cortical ribbon & BG), hypercellular lesions (abscess, primary CNS lymphoma, acute seizures)

65
Q

SWI (Susceptibility-weighted images) & Gradient Echo

A

Mostly used to evaluate blood, which is dark on these (calcification is also dark in these)

Useful for identifying microhemorrhages (like in the evaluation of cerebral amyloid angiopathy)

Great for picking up DAI

66
Q

MR spectroscopy

A

Evaluates brain metabolites, N-acetyl aspartate (NAA) & choline (Cho)

NAA is a measure of neuronal health- higher NAA the healthier the neurons

Choline is a marker of membrane turnover

Decreased NAA & increased Cho –> glial neoplasm. Normally NAA peak towers over Cho & the angle (Hunter’s angle) between them is 45 degrees. In glial neoplasms, Cho becomes equal or higher than NAA

Increased NAA –> Canavan’s disease

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