CORTEX + BASIC ANATOMY
1. Which lobe is primarily responsible for:
a) Impulse control and judgment
b) Visuospatial processing and right–left orientation
c) Language comprehension
d) Primary visual processing
a) Frontal lobe (orbitofrontal cortex)
The orbitofrontal cortex is classic for personality and inhibition.
b) Parietal lobe
The parietal lobes handle body in space (visuospatial) and left–right orientation.
c) Temporal lobe (Wernicke’s area)
Wernicke’s area in the temporal lobe is key for understanding spoken language.
d) Occipital lobe (primary visual cortex)
The occipital lobes house the primary visual cortex, where visual information first arrives from the optic radiations.
What is the typical MoCA score range seen in Mild Cognitive Decline vs Alzheimer’s disease?
MCI: average around 22–23
AD: average around 16–17
MCI is milder, scores are reduced but not as low as in established Alzheimer’s which reflects early but not pervasive cognitive decline
A lesion in the cerebellopontine angle would be expected to affect which cranial nerves/structures and cause what hallmark signs?
Affects CN VII and VIII plus cerebellar connections
Signs: unilateral hearing loss, vertigo and nystagmus, facial weakness, and ipsilateral limb ataxia
The cerebellopontine angle is where the facial and vestibulocochlear nerves enter the brainstem near cerebellar peduncles, so tumors (ex. acoustic neuromas) cause these symptoms
A 62-year-old man speaks in fluent but nonsensical phrases and cannot follow simple commands. Diagnosis and lesion?
Diagnosis: Wernicke’s aphasia
Lesion: left posterior superior temporal gyrus
Fluent jargon speech + poor comprehension + inability to follow commands is the characteristic triad of Wernicke’s
A 52-year-old develops blurred vision, diplopia, dilated unreactive pupils, hoarse voice, neck weakness, and autonomic symptoms after eating home-canned food. EMG shows incremental response with repetitive stimulation. Diagnosis and mechanism?
Diagnosis: Botulism
Mechanism: toxin cleaves SNARE proteins, preventing presynaptic Ach vesicle release at both nicotinic and muscarinic synapses
Autonomic features (pupillary, GI) plus descending paralysis after canned food is classic; incremental EMG response occurs because high-frequency stimulation temporarily overcomes some presynaptic block
Damage to which specific cortical area produces Broca’s aphasia, and what are the main features?
Lesion in the inferior frontal gyrus of the dominant hemisphere (classically left).
Symptoms: non-fluent, effortful, telegraphic speech with relatively preserved comprehension but impaired repetition.
Broca’s area is the “motor speech” region. Patients know what they want to say but can’t fluently produce language. Because the lesion is anterior, comprehension (a temporal lobe function) is often relatively spared, but the motor programming of speech is impaired.
Orientation on the MoCA has high sensitivity but low specificity for which condition?
Primarily dementia and also delirium.
Disorientation is common in both chronic (dementia) and acute (delirium) global brain dysfunction. Suggests cognitive impairment, but it doesnt tell you which cause
What sensory modalities are carried by the Dorsal Column vs the Spinothalamic Tract and where does each tract cross?
Dorsal Column: proprioception, vibration, fine touch. Ascends ipsilaterally and crosses in the medulla
Spinothalamic: pain and temperature. Crosses within 1–2 segments in the spinal cord soon after entry
This explains why a spinal cord lesion can cause ipsilateral loss of vibration/proprioception but contralateral loss of pain/temperature below the level
A 54-year-old man has resting tremor that improves with movement, shuffling gait, rigidity, drooling, and masked facies. Diagnosis and key deep structure?
Diagnosis: Parkinson’s disease
Structure: Substantia nigra pars compacta (dopaminergic neurons)
Nigrostriatal dopamine loss increases inhibitory output of basal ganglia, producing bradykinesia, rigidity, and classic resting tremor
A 23-year-old has numbness in the 4th and 5th digits and weakness of finger abduction/adduction. Where is the lesion and what nerve is involved?
Lesion: Ulnar nerve entrapment at the elbow (cubital tunnel)
Nerve: Ulnar nerve
The ulnar nerve supplies sensation to the 4th/5th digits and intrinsic hand muscles (interossei). Entrapment at the elbow produces the classic “ulnar claw” pattern and sensory changes
Lesions of the right parietal lobe often cause what classic syndrome affecting attention to space?
Left hemispatial neglect
Each parietal lobe attends to the opposite side of space. Damage to the right parietal causes neglect of the left space, patients may ignore the left side of the plate, fail to dress the left side of the body, or only write on the right side of the page.
On the MoCA, patients with Lewy Body Dementia tend to perform especially poorly on which visuospatial/executive task compared to AD, and relatively better on which memory domain?
Especially poor on clock drawing and other visuospatial/executive tasks. Relatively better on delayed recall compared to AD early on.
LBD emphasizes visual hallucinations and visuospatial/executive deficits, with memory not as devastated early as in AD, so the pattern on MoCA can help differentiate
A medullary lesion affecting the dorsal column pathway will cause proprioception/fine touch deficits on which side?
On the contralateral side of the body
In the medulla the dorsal column fibers have already crossed (as internal arcuate fibers) to form the medial lemniscus, so a central lesion there affects contralateral proprioception and fine touch
An 85-year-old with parkinsonian features develops vertical gaze palsy (then horizontal too) but has preserved oculocephalic reflex. What is the diagnosis?
Progressive Supranuclear Palsy (PSP)
“Supranuclear” means the brainstem nuclei and reflexes are intact; the problem is in the higher gaze centers, so doll’s-eye (oculocephalic) reflex remains intact despite voluntary gaze paralysis
Name two key clinical findings that help distinguish Guillain–Barré Syndrome from transverse myelitis.
GBS: pure LMN signs (areflexia, no Babinski), no clear sensory level, peripheral nerve demyelination on NCS, CSF with high protein but normal cell count.
Transverse myelitis: UMN signs (hyperreflexia, Babinski), often a sensory level, spinal cord lesion on MRI, and prominent bowel/bladder involvement.
GBS is a peripheral neuropathy, transverse myelitis is a central cord lesion. UMN vs LMN signs and the presence of a sensory level are key differentiators.
The basal ganglia are composed of which structures? Name the four main parts
Striatum: caudate nucleus, putamen, nucleus accumbens
Globus pallidus (internal and external segments)
Subthalamic nucleus
Substantia nigra
Deep nuclei form loops with cortex and thalamus to help initiate, modulate and terminate movements, as well as influence habit formation and some aspects of motivation and emotion
Patients with Major Depressive Disorder can have abnormal MoCA scores. What general pattern of deficits do they show?
Global cognitive slowing with worse performance on visuospatial/executive tasks, repetition, Letter F fluency, serial 7s, and delayed recall (before cues), but not as severely impaired as in AD/FTD.
Depression often produces a “pseudodementia” picture with slowed processing and poor effort/attention, rather than focal neurodegenerative patterns.
A lesion of the spinothalamic tract in the spinal cord above the level where fibers enter will cause what sensory loss?
Contralateral loss of pain and temperature below the lesion
Because spinothalamic fibers cross early (at or near their entry level), a lesion laterally in the cord hits already-crossed fibers carrying opposite-side pain/temperature
A 55-year-old female cannot write, calculate, or distinguish her fingers. What syndrome is this and where is the lesion?
Syndrome: Gerstmann syndrome
Lesion: left parietal lobe, especially the angular gyrus
The tetrad is dysgraphia, dyscalculia, finger agnosia, and left–right disorientation (left parietal “Gerstmann” cluster)
A patient has both UMN and LMN signs (hyperreflexia + Babinski, plus fasciculations and muscle atrophy) with preserved sensation. Diagnosis and primary area involved?
Diagnosis: Amyotrophic Lateral Sclerosis (ALS)
Area: degeneration of anterior horn cells (LMN) and corticospinal tracts (UMN)
The mix of UMN and LMN signs with normal sensation is classic for ALS. It selectively affects motor pathways, sparing sensory tracts
Give at least three movement or neuropsychiatric disorders associated with basal ganglia dysfunction
1. Parkinson’s disease
2. Huntington’s disease
3. Tourette’s syndrome
4. Dystonia
5. OCD
6. Tardive dyskinesia
7. Some forms of cerebral palsy (movement aspects)
Basal ganglia modulates movement and also contributes to “gating” of thoughts and behaviors. Too little movement (hypokinetic, like Parkinson’s) or too much movement (hyperkinetic, like chorea, tics or dystonia).
In Parkinson’s Disease Dementia, early cognitive changes are mainly due to disruption of what circuit, and which domains are often affected first?
Disruption of frontal–striatal circuits
Early deficits in executive function and attention (e.g., clock drawing, attention tasks, verbal fluency, abstraction)
PD is fundamentally a basal ganglia disease that secondarily impairs frontal functions via disrupted loops, showing up on tasks with high executive demand.
Which three MoCA subtests related to attention are most often impaired in delirium?
Letter A Tapping
Serial 7 Subtractions
Digit Span Backward
Delirium is defined by impaired attention. These tasks all require sustained and focused attention, so they are very sensitive to delirious states
A 48-year-old with HTN has vertigo, nystagmus, hoarseness, ipsilateral facial pain/temp loss, contralateral body pain/temp loss, ataxia, and hiccups. Diagnosis and artery?
Diagnosis: Lateral medullary (Wallenberg) syndrome
Artery: Posterior Inferior Cerebellar Artery (PICA)
Wallenberg involves spinothalamic (contralateral body pain/temp), spinal trigeminal (ipsilateral face pain/temp), nucleus ambiguus (hoarseness/dysphagia), vestibular nuclei (vertigo/nystagmus), cerebellar connections (ataxia), and sympathetics (Horner)
For each disorder, is the problem pre- or post-synaptic, and what part of the NMJ is affected?
a) Botulism
b) Lambert–Eaton Myasthenic Syndrome
c) Myasthenia Gravis
a) Botulism – pre-synaptic, blocks Ach release from presynaptic terminals
b) Lambert–Eaton – pre-synaptic, antibodies against voltage-gated Ca²⁺ channels, impairing Ach release
c) Myasthenia Gravis – post-synaptic, IgG antibodies against Ach receptors
All three affect neuromuscular transmission but at different levels: botulism and LEMS reduce Ach release; MG blocks the receptors. That explains the different EMG patterns and autonomic involvement