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from Guyton and Hall Textbook of Medical Physiology (4th South Asia Edition) write a proper 5 mark short note on lesions of internal capsule

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Lesions of the Internal Capsule (Guyton & Hall – 5 Mark Short Note)

Anatomy (brief): The internal capsule is a compact band of white matter lying between the caudate nucleus and putamen of the basal ganglia. It carries the corticospinal (pyramidal) tract and other descending/ascending fibers connecting the cerebral cortex with the brain stem and spinal cord. The corticospinal tract, after leaving the motor cortex, passes through the posterior limb of the internal capsule (between the caudate nucleus and putamen) before descending through the brain stem to form the pyramids of the medulla - Guyton and Hall Textbook of Medical Physiology.
Cause of lesion: The internal capsule is a common site of damage in stroke, caused either by:
  • Hemorrhage from a ruptured blood vessel, or
  • Thrombosis of a major artery supplying this region.
Because the corticospinal fibers are tightly packed together as they pass through this narrow region, even a small lesion here produces widespread and severe motor deficits - much greater than an equivalent-sized cortical lesion, since nearly all fibers from a large area of motor cortex converge and pass through this small space.
Effects of internal capsule lesion:
  1. Contralateral hemiplegia - paralysis of the opposite side of the body, since the corticospinal fibers have not yet crossed at this level (decussation occurs later in the medulla).
  2. Loss of voluntary control of fine, discrete movements, especially of the hands and fingers, due to interruption of the pyramidal (area pyramidalis) fibers.
  3. Muscle spasticity (hypertonia): Most capsular lesions (especially from stroke) damage not only the corticospinal tract but also adjacent nonpyramidal (extrapyramidal) accessory pathways. These pathways normally inhibit the vestibular and reticular brain stem motor nuclei. When this inhibition is lost ("disinhibition"), the vestibular and reticular nuclei become spontaneously overactive, producing spastic paralysis with increased muscle tone on the affected side - a hallmark of capsular/pyramidal stroke.
  4. Initially there may be a transient phase of flaccidity/hypotonia (loss of tonic cortical stimulatory effect on cord motor neurons) before spasticity sets in as reflex mechanisms take over.
Clinical correlation: This combination - contralateral hemiplegia with spasticity and loss of fine motor control - is the classic picture seen in patients after a capsular stroke (a common cause of hemiplegia in clinical practice), reflecting simultaneous involvement of the pyramidal and adjacent extrapyramidal pathways within the narrow confines of the internal capsule.
Source: Guyton and Hall Textbook of Medical Physiology, Chapter on "Cortical and Brain Stem Control of Motor Function" - section "Effect of Lesions in the Motor Cortex or in the Corticospinal Pathway."
A quick check of recent systematic reviews (PMIDs 38185754, 35343284, 37260605) on capsular/pyramidal stroke did not reveal any findings that contradict this core physiological description - they mainly address imaging scoring and rare stroke etiologies, not the basic capsular lesion physiology described above.
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