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INTERNAL CAPSULE Tutorial Skenario D Blok 15

Internal Capsule

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Kapsula Interna

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Page 1: Internal Capsule

INTERNAL CAPSULE

Tutorial Skenario D Blok 15

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TYOE OF FIBERS

• Anterior limb: frontopontine fibers (frontal cortex to pons), thalamocortical fibers (thalamus to frontal lobe)

• Genu (angle): corticobulbar fibers (cortex to brainstem)

• Posterior limb: corticospinal fibers (cortex to spine), sensory fibers

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BLOOD SUPPLY

• Anterior limb: mainly fed by the lenticulostriate branches of middle cerebral artery(MCA), less often branches of anterior cerebral artery (ACA)

• The lenticulostriate arteries are small penetrating blood vessels that supply blood flow to most of the subcortical structures.

• Genu: lenticulostriate branches of MCA• Posterior limb: lenticulostriate branches of MCA &

anterior choroidal artery (AChA) of internal carotid artery

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• An extremely important point to remember is that because of the small size of the internal capsule a very small lesion can produce the same deficit as a very large lesion in the cerebral hemisphere.

• Lesions in the internal capsule are very common, especially from blockage of the internal carotid and middle cerebral arteries or their branches, and from hemorrhage from the striate arteries.

• Hemorrhage from the striate (lenticulostriate) arteries damages a larger area of the internal capsule and adjacent structures than supplied by these arteries. Because the striate/lenticulostriate arteries are so susceptible to hemorrhage (primarily in people with hypertension), they have been referred to as the “arteries of stroke”.

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PROJECTION FIBERS• These are fibers which connect the cortex to other areas in the brain stem & the spinal cord.

• Projection fibers are 2 types:• A- Ascending (afferent),or

corticopetal:• Conveying fibers to the

cortex• 1- Thalamic radiation:

connecting different thalamic nuclei with different parts of cortex.

• 2- Optic radiation.• 3- Auditory radiation.

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PROJECTION FIBERS• B- Descending (Efferent), or corticofugal:

• 1. Pyramidal: a. Corticospinal. b. Corticobulbar.

• 2. Corticopontine.

• 3. Corticoreticular.

• 4. Corticorubral

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INTERNAL CAPSULE• Thick band of projection fibers.

• V-shaped with its concavity directed laterally in horizontal section

• Its concavity is related to Lentiform nucleus.

• It is formed of:• Anterior limb.• Genu.• Posterior limb.

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INTERNAL CAPSULE• Anterior limb:• Between head of caudate

nucleus & lentiform nucleus.• It contains:• 1-Anterior thalamic

radiation: From anterior & mediodorsal

thalamic nuclei, to the frontal cortex.

• 2-Frontopontine fibers: That project to pontine nuclei, in the basal part of the Pons.

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INTERNAL CAPSULE• Genu of internal capsule:• Is the angle of the V which

points medially, between head of caudate nucleus and thalamus.

• It contains:• 1- Corticonuclear (Corticobulbar).• 2- Anterior part of sensory

(superior thalamic) radiation, from ventral anterior & ventral lateral nuclei to motor regions of the frontal lobe.

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INTERNAL CAPSULE• Posterior limb:• A-Lenticothalamic part• Lies between thalamus &

lentiform nucleus.• Contains:• 1-Corticospinal fibers.• 2-Frontopontine.• 3-Frontorubral.• 4-Great part of sensory

(superior thalamic ) radiation, from the ventral posterior nucleus to the primary somatosensory cortex.

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INTERNAL CAPSULE• B-Retrolentiular part:

• It contains fibers from medial & lateral geniculate nuclei of thalamus, which form the auditory & optic radiation.

• Optic radiation passes to visual cortex, around the calcarine sulcus (geniculoalcarine fibers).

• Auditory radiation passes to superior temporal gyrus.

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• Lacunes are caused by occlusion of a single deep penetrating artery that arises directly from the constituents of the Circle of Willis, cerebellar arteries, and basilar artery. The corresponding lesions occur in the deep nuclei of the brain (37% putamen, 14% thalamus, and 10% caudate) as well as the pons (16%) or the posterior limb of the internal capsule (10%). They occur less commonly in the deep cerebral white matter, the anterior limb of the internal capsule, and the cerebellum.

• The two proposed mechanisms are microatheroma and lipohyalinosis. At the beginning, lipohyalinosis was thought to be the main small vessel pathology, but microatheroma now is thought to be the most common mechanism of arterial occlusion (or stenosis). Occasionally, atheroma in the parent artery blocks the orifice of the penetrating artery (luminal atheroma), or atheroma involves the origin of the penetrating artery (junctional atheroma).

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• Alternatively, hypoperfusion is believed to be the mechanism when there is stenosis of the penetrating artery. When no evidence of small vessel disease is found on histologic examination, an embolic cause is assumed, either artery-to-artery embolism orcardioembolism. In one recent series, 25% of patients with clinical radiologically defined lacunes had a potential cardiac cause for their strokes.

• Advanced age, chronic hypertension, smoking and diabetes mellitus are risk factors. It is unclear whether there is an association with alcohol consumption, elevated cholesterol, or history of prior stroke. Lacunar strokes may result from carotid artery pathology or microemboli from the heart as in atrial fibrillation. Patients often recover well, but if there is enough white matter disease from lacunar pathology, one can see a subcortical dementia such as Binswanger disease.

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• If a patient has weakness +/- sensory deficits, how can you tell whether the stroke is subcortical or cortical? What other symptoms or signs can help you localize the stroke to the internal capsule as opposed to the cortex?

• A patient who presents with arm and leg weakness may have either a small internal capsule stroke or a large ACA + MCA cortical stroke. Looking at the homunculus in the figure above, the cortical leg area is supplied by the ACA and the arm area is supplied by the MCA. However, the injury to the cortices produces other symptoms and signs that not commonly produced by injury to the subcortical areas.

• The presence of these cortical signs may exclude an internal capsule stroke:• gaze preference or gaze deviation• expressive or receptive aphasia• visual field deficits• visual or spatial neglect• If any of these signs are present, the patient may have a cortical stroke, not

an internal capsule stroke.