Neuroanatomy/Pathology- Berkowitz Flashcards
1
Q
Examination of mental status includes:
A
- Level of consciousness
- Integrity of individual cognitive functions (attention, memory, language, calculation, abstract reasoning, praxis)
2
Q
What areas of brain control consciousness?
A
RAS, thalami, & cerebral hemispheres
3
Q
What is delirium?
A
Fluctuating acute confusion
4
Q
What is lethargy/somnolence?
A
Falling asleep without repetitive stimulation
5
Q
What is being stuporous?
A
Requiring painful and/or painful physical stimulation to be awakened
6
Q
What is obtundation?
A
Between somnolent & stuporous
7
Q
What domain of cognitive assessment should be done first, because if not in tact, the rest cannot be tested?
A
Attention
8
Q
What lobes control attention?
A
Frontal & parietal
9
Q
Examples of testing attention
A
- Digit span- recite a string of #’s backward & forwards
- Months backwards
- Spell “world” backwards
- Serial 7’s
10
Q
What is a core feature of delirium?
A
Inattention
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)
12
Q
What lobe provides ability for memory?
A
Temporal lobe
13
Q
Even with profound memory loss, people should remember their name. If they cannot, it is usually:
A
Psychiatric
14
Q
Testing short term memory
A
Give 3 words to recite & remember & ask them to repeat 5 minutes later
15
Q
Why does amnesia usually occur?
A
Damage to one or both temporal lobes, specifically medial temporal lobe- hippocampus
16
Q
Deficits in memory are core features of:
A
- Alzheimer’s
- Transient global amnesia
17
Q
What lobes provide language?
A
Frontal & temporal lobes (most commonly in left hemisphere)
18
Q
What hemisphere usually controls language?
A
Left (for all right-handed people & most left-handed people)
19
Q
Where is Broca’s area?
A
Left inferior frontal gyrus
20
Q
Where is Wernicke’s area?
A
Left posterior superior temporal gyrus
21
Q
Bedside tests that test cognitive function across multiple domains
A
- MMSE (mini-mental state examination)
- MoCA (Montreal cognitive assessment)
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
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)
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
25
Oculomotor, Trochlear, & Abducens nerves
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
26
Trigeminal nerve
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
27
Facial nerve
Tested by asking patients to raise eyebrows & close eyes tightly (upper facial muscles); smile for lower facial muscles
28
Vestibulocochlear nerve
Hearing: sound from exterior > inner ear > nerve > brainstem & thalamus > auditory cortex in superior temporal lobe
29
Glossopharangeal & Vagus nerves
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
Spinal accessory nerve
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
Hypoglossal nerve
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
Motor system
Brain > brainstem > spinal cord > ventral nerve roots > peripheral nerves > NMJ > muscle
33
Paresis vs plegia
Paresis: weakness
Plegia: paralysis
34
What is trigeminal neuralgia commonly caused by?
Compression via superior cerebellar artery pulsating directly on nerve
35
Sensory exam
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
Tested reflexes
Biceps: C5-6
Brachioradialis: C6
Triceps: C7-8
Patellar: L3-4
Ankle/achilles: S1-2
37
If you need to elicit reflexes via Jendrassik maneuver or other type of assistance:
Hyporeflexia is present (or not relaxed)
38
Sign of hyper-reflexia
Spread of reflex from one tested area to an adjacent area (eliciting biceps causes simultaneous finger flexion or eliciting patellar causes ankle plantarflexion)
39
Pathologic reflexes
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
Exams for coordination
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
Ataxia
Uncoordinated movements
42
Dysmetria
Inaccuracy of movements (under or overshooting target)
43
Dysdiadochokinesia
Uncoordinated RAM
44
Why does ataxia, dysmetria, or dysdiadochokinesia occur?
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
Parkinsonian gait
Stooped, small-stepped, shuffling gait with difficulty turning
46
Magnetic gait
Feet lifted briefly off the ground before being returned briskly to ground seen in NPH & with proprioception dysfunction
47
Ataxic gait
Wide-based & unsteady gait seen in cerebellar dysfunction (like being drunk) & severe proprioception dysfunction
48
Spastic gait
Leg extended, foot plantarflexed, entire leg circumducted with each step. If both legs are spastic --> scissoring. Seen with CNS dysfunction of motor system
49
Does bacterial or viral/fungal infection abscess in brain appear more acutely clinically?
Bacterial; viral/fungal can take a few days to show itself
50
Why is CT not great when evaluating posterior fossa?
Beam-hardening artifact
51
Does MRI have radiation exposure?
No
52
CT vs MRI
MRI takes longer, more expensive, cannot be performed in patients with ferromagnetic device in body, or exposure to shrapnel
53
Can CT or MRI use different windows to highlight different portions of an image?
CT
54
How does CT work?
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
Causes of hyperdensity on CT
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
Causes of hypodensity on CT
Any pathology that causes edema:
- Tumor
- Inflammation
- Infection
- Trauma
- Ischemic CVA (after acute phase)
Sequelae of prior injury (trauma, infarct, demyelinating lesion)
57
Ischemic CVA vs other causes of hypodensity on CT
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
MRI sequences to evaluate brain
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
T1-weighted images
Gray matter is darker than white matter
CSF is dark
60
T2-weighted images
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
FLAIR
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
General use for T1 vs T2/FLAIR
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
Appearance of blood on MRI depending on age
T1:T2
Hyperacute- Isointense:Hyperintense
Acute- Isointense:Hypointense
Early subacute- Hyper:Hypo
Late subacute- Hyper:Hyper
Chronic- Hypo:Hypo
64
DWI & ADC
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
SWI (Susceptibility-weighted images) & Gradient Echo
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
MR spectroscopy
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
