AN62.1-6 | Cranial nerve nuclei & Cerebral hemispheres — Summary & Reflection

REFLECT

Return to the three patients:

1. Patient A: Left MCA infarct. He has right arm + face weakness but right leg power is NORMAL. Which part of the motor cortex/internal capsule is spared?
2. Patient B (Parkinson's): The dopaminergic nigrostriatal pathway is lost. Does this enhance the DIRECT or INDIRECT basal ganglia pathway? How does this lead to bradykinesia?
3. Patient C: Right subthalamic nucleus infarct → left hemiballismus. Trace the pathway: why does loss of STN cause violent involuntary movements on the CONTRALATERAL side?

Discussion: (1) Leg area is medial on motor cortex (ACA territory); right leg spared = ACA intact; MCA supplies arm + face (lateral). (2) Dopamine deficiency: activates D2 (inhibitory) → reduces direct pathway activation; also inhibits D1 → reduces direct pathway → INDIRECT pathway dominant → bradykinesia, rigidity. (3) STN normally drives GPi via indirect pathway; STN loss → GPi underactive → thalamus DISINHIBITED → excessive motor cortex activation → violent contralateral movements.

KEY TAKEAWAYS

Key Takeaways — Cerebral Hemisphere, Basal Ganglia, Circle of Willis

• Motor areas: Area 4 (primary motor), Area 6 (premotor/SMA), Broca's 44/45 (speech motor — left)
• Sensory areas: Areas 1,2,3 (somatosensory), Area 17 (visual), Areas 41/42 (auditory), Area 22 (Wernicke's)
• Internal capsule: Anterior limb (frontopontine), Genu (corticobulbar), Posterior limb (corticospinal + somatosensory)
• Basal ganglia: Direct (facilitatory via D1) and Indirect (inhibitory via D2 + STN) pathways; Parkinson = indirect dominant; Hemiballismus = STN loss
• Thalamus VPL/VPM = body/face sensation relay; VL = cerebellar/basal ganglia motor relay; LGN/MGN = vision/hearing
• Circle of Willis: AComm (most common aneurysm), PComm (CN III compression), MCA (most common stroke territory in India)