Internal capsule and basal ganglia
Internal capsule, basal ganglia and thalamus: anatomy, circuits and lesions
Internal capsule, basal ganglia and thalamus for FCPS Part 1: capsule fibres and supply, direct and indirect loops, dopamine and thalamic nuclei. Explains Parkinson, Huntington, hemiballismus, Sydenham chorea, deep brain stimulation targets and thalamic strokes.
Position of the internal capsule
- The internal capsule is a V-shaped sheet of white matter seen in horizontal section. It lies lateral to the thalamus and caudate nucleus and medial to the lentiform nucleus (putamen and globus pallidus).
- Because motor and sensory fibres for the whole opposite half of the body are packed into this narrow band, a small lesion causes a dense contralateral hemiplegia affecting face, arm and leg together.
| Part | Contents | Blood supply |
|---|---|---|
| Anterior limb | Frontopontine fibres, anterior thalamic radiation | Medial striate (recurrent artery of Heubner, ACA) |
| Genu | Corticobulbar fibres (face and head) | Lenticulostriate (MCA), direct ICA branches |
| Posterior limb | Corticospinal (arm in front, leg behind), sensory thalamocortical radiation | Lenticulostriate (MCA), anterior choroidal |
| Retrolentiform part | Optic radiation | Anterior choroidal, PCA branches |
| Sublentiform part | Auditory radiation | Anterior choroidal |
- Lacunar infarct in the posterior limb gives pure motor hemiplegia of face, arm and leg equally. A patient who can still close both eyes but has dense right hemiplegia has a left internal capsule lesion: upper facial muscles have bilateral cortical supply.
- Hypertensive haemorrhage comes from rupture of Charcot–Bouchard microaneurysms on the lenticulostriate arteries ("arteries of cerebral haemorrhage"). The commonest site is the putamen, then the thalamus, pons and cerebellum.
Basal ganglia: parts
- Striatum = caudate + putamen. Lentiform nucleus = putamen + globus pallidus. Also the subthalamic nucleus and substantia nigra (pars compacta, dopaminergic; pars reticulata, output like the GPi).
- The nigrostriatal pathway uses dopamine. Striatal output neurones use GABA. Subthalamic neurones are glutamatergic (excitatory). The output nuclei (GPi, SNr) tonically inhibit the thalamus with GABA.
Direct and indirect pathways
| Step | Direct pathway (D1) | Indirect pathway (D2) |
|---|---|---|
| Cortex excites | Striatal neurones with D1 receptors | Striatal neurones with D2 receptors |
| Striatum inhibits | GPi and SNr | GPe |
| Next | GPi inhibition of thalamus is reduced | GPe stops inhibiting STN, so STN excites GPi more |
| Thalamus | Released | More strongly inhibited |
| Net effect | Movement increased | Movement reduced |
| Dopamine (nigra) | Excites (D1) | Inhibits (D2) |
- Dopamine therefore favours movement through both receptors. Loss of dopamine leaves the indirect pathway dominant: the subthalamic nucleus becomes overactive, the GPi fires excessively, and excess pallidal inhibition of the thalamus causes bradykinesia and rigidity. Deep brain stimulation of the STN (or GPi) in Parkinson disease aims to reduce this outflow.
- Destroying the STN does the opposite: GPi output falls, the thalamus is disinhibited, and violent flinging movements follow (hemiballismus).
Movement disorders
| Disorder | Lesion | Features |
|---|---|---|
| Parkinson disease | Loss of dopaminergic neurones in substantia nigra pars compacta | Resting tremor, cogwheel rigidity, bradykinesia, postural instability; Lewy bodies (alpha-synuclein) |
| Huntington disease | Caudate (and putamen) GABAergic neurones; CAG repeat on chromosome 4, autosomal dominant with anticipation | Chorea, dementia, depression and behavioural change |
| Hemiballismus | Contralateral subthalamic nucleus, usually lacunar stroke | Wild flinging of proximal limbs |
| Sydenham chorea | Antibodies against basal ganglia neurones after group A streptococcal throat infection (molecular mimicry) | Chorea, clumsy handwriting, emotional lability, months after the sore throat; stops in sleep |
| Wilson disease | Copper in lentiform nucleus | Tremor, dystonia, dysarthria, Kayser–Fleischer rings, low caeruloplasmin |
| Kernicterus | Unconjugated bilirubin stains basal ganglia (globus pallidus) in neonates | Severe neonatal jaundice (e.g. Rh haemolytic disease); later athetoid cerebral palsy, deafness |
| Tardive dyskinesia | Long-term D2 blockade | Orofacial dyskinesia |
- In Huntington disease loss of striatal GABA neurones releases the pallidum and nigra from inhibition; the indirect pathway is lost first, so movement is excessive.
- Sydenham chorea may be the only major Jones criterion and may appear when the ASO titre is falling; echocardiography should still be done.
Thalamus
The thalamus relays all sensation except smell, and links cerebellum and basal ganglia to motor cortex.
| Nucleus | Input | Output |
|---|---|---|
| VPL | Medial lemniscus, spinothalamic (body) | Somatosensory cortex |
| VPM | Trigeminal lemniscus (face) and taste (from nucleus tractus solitarius) | Somatosensory and gustatory cortex |
| LGB | Optic tract | Visual cortex |
| MGB | Inferior colliculus | Auditory cortex |
| VL, including the ventral intermediate (Vim) part | Dentate nucleus of cerebellum (and basal ganglia) | Motor cortex |
| VA | Basal ganglia | Premotor cortex |
| Anterior | Mammillothalamic tract | Cingulate gyrus (Papez circuit) |
| Dorsomedial | Amygdala, olfactory, limbic | Prefrontal cortex; damaged in Korsakoff syndrome |
| Pulvinar | Visual association areas | Parietal and occipital cortex |
- Deep brain stimulation for essential tremor targets the Vim nucleus, the relay of cerebellar (dentate) output to motor cortex. VPL and VPM are purely sensory relays.
Thalamic vascular lesions
- Thalamic haemorrhage: contralateral sensory loss greater than weakness (adjacent capsule), eyes deviated downwards and inwards ("looking at the nose") because the bleed presses on the dorsal midbrain vertical gaze centres, and small poorly reactive pupils.
- Thalamic pain (Dejerine–Roussy) syndrome: after a VPL infarct (thalamogeniculate branches of the PCA), the numb half of the body later develops severe burning pain.
- Artery of Percheron: a single variant branch from one PCA (P1 segment) that supplies both paramedian thalami and the rostral midbrain. Its occlusion gives drowsiness or coma, vertical gaze palsy and memory loss. Deep cerebral venous thrombosis can mimic it.
Remember Dopamine loss makes the STN and GPi overactive and clamps the thalamus; STN destruction releases it.
Exam trap In Parkinson disease the subthalamic nucleus is overactive; in hemiballismus it is destroyed.
Exam trap Essential tremor stimulation targets the Vim (cerebellar relay), not the sensory VPL or VPM.
How FCPS asks about this
- Thalamic nucleus relaying taste: VPM.
- Eyes deviated down and in, small pupils, sensory loss more than weakness: contralateral thalamic haemorrhage.
- Bilateral paramedian thalamic infarcts from one vessel: artery of Percheron.
- Chorea after a sore throat in a child: antibodies against basal ganglia neurones (Sydenham chorea).
- Aim of STN stimulation in Parkinson disease: reduce excess pallidal inhibition of the thalamus.
- Hemiballismus: contralateral subthalamic nucleus.
- Neurotransmitter of nigrostriatal pathway: dopamine; Huntington disease loses striatal GABA neurones.
Test yourself on this topic
5 of the 34 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
Which fibres pass through the genu of the internal capsule?
Answer: Corticobulbar fibres
From front to back: the anterior limb carries frontopontine and thalamocortical fibres; the genu carries corticobulbar fibres to cranial nerve motor nuclei; the posterior limb carries corticospinal fibres (arm in front of leg) and sensory thalamocortical fibres; the retrolenticular and sublenticular parts carry the optic and auditory radiations.
Capsule map
- Anterior limb: frontopontine
- Genu: corticobulbar
- Posterior limb: corticospinal, sensory
- Behind: optic, auditory radiations
Remember Genu for the face (cranial nerves).
Exam trap Upper motor neurone facial weakness spares the forehead.
Why the other options are wrong
- Corticospinal fibres to the leg Posterior limb.
- Optic radiation Retrolenticular part.
- Auditory radiation Sublenticular part.
- Frontopontine fibres Anterior limb.
A 66-year-old man with Parkinson disease has slowness and difficulty starting movements. Which change in basal ganglia output best explains his bradykinesia?
Answer: Increased GPi inhibition of the thalamus
Dopamine from the substantia nigra excites the direct pathway through D1 receptors and inhibits the indirect pathway through D2 receptors; both effects normally reduce the output of the internal globus pallidus. When nigral neurons are lost, the direct pathway weakens and the indirect pathway, including the subthalamic nucleus, becomes overactive. The internal globus pallidus then inhibits the motor thalamus excessively, so thalamocortical drive falls and movement is slow to start.
Parkinson circuitry
- Loss of nigral dopamine
- Direct pathway weak, indirect strong
- GPi output rises
- Thalamus inhibited, movement slow
Remember Parkinson disease: too much pallidal brake on the thalamus.
Exam trap Subthalamic deep brain stimulation helps because it reduces this overactive output.
Why the other options are wrong
- Reduced GPi inhibition of the thalamus This pattern produces excess movement, as in chorea.
- Increased dopamine at striatal D1 receptors Dopamine is reduced, not increased.
- Reduced subthalamic nucleus activity The subthalamic nucleus becomes overactive.
- Increased cortical drive to the striatum Not the main change in Parkinson disease.
A 55-year-old woman is found deeply drowsy but rousable, with impaired vertical gaze and poor memory on waking. MRI shows symmetrical infarcts in both paramedian thalami and the rostral midbrain. Occlusion of which single vessel explains both sides being affected?
Answer: Artery of Percheron
The paramedian thalami are normally supplied by thalamoperforating branches from each P1 segment of the posterior cerebral artery. In some people a single trunk, the artery of Percheron, arises from one P1 and supplies both sides. Its occlusion infarcts both paramedian thalami, often with the rostral midbrain, causing reduced consciousness from loss of reticular activating relays, vertical gaze palsy and memory disturbance. Imaging may be normal early, so the diagnosis is easily missed.
Artery of Percheron
- Single trunk from one P1
- Supplies both paramedian thalami
- Drowsiness, vertical gaze palsy
- Memory loss
Remember Bilateral paramedian thalamic infarcts: artery of Percheron.
Exam trap Bilateral thalamic lesions can also come from deep venous thrombosis, so check the internal cerebral veins.
Why the other options are wrong
- Basilar tip Occlusion would also affect the occipital lobes, cerebellum and brainstem widely.
- Anterior choroidal artery Unilateral; supplies the internal capsule and optic tract.
- Posterior communicating artery Unilateral; its branches supply the anterior thalamus.
- Superior cerebellar artery Supplies the upper pons and cerebellum.
A 58-year-old woman has dense left hemiplegia, left hemisensory loss and a left homonymous hemianopia, but no aphasia, neglect or confusion. MRI shows an infarct in the posterior limb of the right internal capsule extending into the optic tract. Which artery is most likely occluded?
Answer: Right anterior choroidal artery
The anterior choroidal artery arises from the internal carotid artery just above the posterior communicating artery. It supplies the posterior limb of the internal capsule, the optic tract, the lateral geniculate body and the choroid plexus of the lateral ventricle. Occlusion gives the triad of contralateral hemiplegia, hemianaesthesia and homonymous hemianopia, without the cortical signs of a large MCA stroke.
Anterior choroidal artery
- Branch of internal carotid
- Posterior limb, optic tract, LGB
- Triad: hemiplegia, hemianaesthesia, hemianopia
- No cortical signs
Remember Three hemi signs and no cortical signs: anterior choroidal.
Exam trap The artery can be injured during clipping of carotid–posterior communicating aneurysms.
Why the other options are wrong
- Right middle cerebral artery Would add cortical signs such as neglect in a right MCA stroke.
- Right posterior cerebral artery Gives hemianopia but usually little weakness.
- Right recurrent artery of Heubner Supplies the caudate and anterior limb.
- Basilar artery Gives brainstem signs, often bilateral.
A 62-year-old man with Parkinson disease has disabling fluctuations despite levodopa and is referred for deep brain stimulation of the subthalamic nucleus. Which of the following abnormalities in the basal ganglia circuit does this aim to correct?
Answer: Excess pallidal inhibition of the thalamus
Loss of nigral dopamine reduces the D1-driven direct pathway and releases the D2-inhibited indirect pathway. The net effect is overactivity of the subthalamic nucleus, which drives the internal globus pallidus (and substantia nigra pars reticulata) to inhibit the motor thalamus too much. With less thalamic drive to the cortex, movement is slow and small. High-frequency stimulation of the overactive subthalamic nucleus reduces this excessive pallidal output.
Parkinson circuit
- Dopamine loss: direct pathway down, indirect up
- Subthalamic nucleus overactive
- GPi over-inhibits the thalamus
- Less cortical drive: bradykinesia
Remember Parkinson: the thalamus is held back by the pallidum.
Exam trap In hemiballismus the subthalamic nucleus is destroyed; in Parkinson disease it is overactive.
Why the other options are wrong
- Reduced activity of the subthalamic nucleus The subthalamic nucleus is overactive in Parkinson disease.
- Excess excitation of the cortex by the thalamus Thalamic drive to the cortex is reduced.
- Overactivity of the direct (D1) pathway The direct pathway is underactive without dopamine.
- Loss of cerebellar input to the motor cortex The cerebellar circuit is not the primary problem.
Where this sits in the CPSP syllabus
- Paper 1: Neuroanatomy, Internal capsule, basal ganglia and thalamus
- Surgery & Allied, Paper 2: Cranium and brain, Internal capsule, basal ganglia and thalamus
- Medicine & Allied, Paper 2: Central nervous system, Internal capsule, basal ganglia and thalamus