Basal ganglia and pituitary
Basal ganglia, thalamus, hypothalamus, pineal and pituitary on imaging
The basal ganglia, thalamus, hypothalamus, pineal and pituitary change signal on CT and MRI in typical ways with metabolic and toxic disease. CPSP asks how they relate to each other, what each nucleus does, and the signature of sellar, suprasellar and pineal masses.
Deep grey matter: anatomy
- Caudate head forms the lateral wall of the frontal horn. Lentiform nucleus = putamen (lateral) + globus pallidus (medial), lying lateral to the internal capsule. Striatum = caudate + putamen.
- From medial to lateral at the level of the thalamus: thalamus, posterior limb of the internal capsule, globus pallidus, putamen, external capsule, claustrum, extreme capsule, insula.
- Subthalamic nucleus lesion (small lacune) gives contralateral hemiballismus.
- Pathways: the nigrostriatal pathway carries dopamine from the substantia nigra pars compacta to the caudate and putamen; its loss causes Parkinson disease. Striatal output neurons use GABA: in Huntington disease the GABAergic neurons of the caudate die first, so the caudate heads atrophy and the frontal horns become box-shaped.
- Hypertensive haemorrhage arises from lenticulostriate arteries (Charcot–Bouchard microaneurysms) and occurs most often in the putamen, then thalamus, pons and cerebellum.
Signal changes in the basal ganglia
| Finding | Cause |
|---|---|
| T1 bright globus pallidus, normal T2 | Manganese deposition in cirrhosis or portosystemic shunting |
| Pallidum and subthalamic nuclei abnormal in a jaundiced neonate | Kernicterus (unconjugated bilirubin); later athetosis, gaze palsy, deafness |
| T1 bright, mildly CT-dense putamen with hemichorea | Non-ketotic hyperglycaemia; not a bleed |
| Dense symmetrical pallidal calcification | Hypoparathyroidism (also incidental in older adults) |
| T2 bright putamina, "giant panda face" in the midbrain; tremor, dysarthria, raised liver enzymes in a teenager | Wilson disease: defective ATP7B copper transporter cannot load copper into caeruloplasmin or bile; Kayser–Fleischer rings are nearly always present once the brain is involved |
| T2 bright putamina and periaqueductal grey, high lactate | Leigh syndrome (mitochondrial failure) |
| Non-enhancing T2 bright foci in pallidum, thalami and cerebellar white matter in a child with café-au-lait macules | NF1 "unidentified bright objects" (myelin vacuolation); follow any that enhance, grow or cause mass effect as a possible glioma |
| Pulvinar brighter than the anterior putamen on FLAIR (pulvinar sign); young adult with months of depression and painful limbs, then ataxia and dementia | Variant CJD (prion from BSE-infected beef) |
| Cortical ribboning and caudate–putamen bright on diffusion | Sporadic CJD |
Thalamus
| Nucleus | Relay |
|---|---|
| VPL | Body touch, proprioception, pain |
| VPM | Face sensation and taste |
| VL and VIM | Cerebellar (dentate) output to motor cortex; VIM is the tremor target for deep brain stimulation |
| Lateral geniculate | Vision |
| Medial geniculate | Hearing |
| Anterior | Limbic memory circuit |
| Dorsomedial | Prefrontal cortex: emotion and memory |
| Pulvinar | Visual association |
- Smell is the only sense with no thalamic relay, so a thalamic stroke spares it.
- Thalamic haemorrhage: sensory loss greater than weakness, eyes deviated down and in, small pupils; later thalamic pain.
- Artery of Percheron: one trunk from a PCA supplying both paramedian thalami and the rostral midbrain: drowsiness, vertical gaze palsy, memory loss. Bilateral thalamic lesions may also be deep venous thrombosis (internal cerebral veins).
Hypothalamus
| Nucleus | Function | Lesion |
|---|---|---|
| Supraoptic and paraventricular | ADH and oxytocin | Diabetes insipidus |
| Ventromedial | Satiety | Hyperphagia and obesity |
| Lateral | Hunger | Anorexia |
| Anterior (preoptic) | Senses warmth; heat loss by sweating and skin vasodilation | Hyperthermia |
| Posterior | Heat conservation and production by vasoconstriction, piloerection and shivering | Poikilothermia |
| Suprachiasmatic | Circadian rhythm | Disturbed sleep–wake cycle |
| Mammillary bodies | Memory circuit | Wernicke–Korsakoff |
- Wernicke encephalopathy (alcohol or prolonged vomiting in pregnancy): T2 bright mammillary bodies, medial thalami and periaqueductal grey. A normal MRI does not exclude it.
- Kallmann syndrome: GnRH neurons fail to migrate from the olfactory placode; hypoplastic olfactory bulbs and anosmia.
- Hypothalamic hamartoma: small non-enhancing mass, isointense to grey matter, hanging from the tuber cinereum; gelastic seizures and precocious puberty.
Pineal region
- Pineal calcification is common in adults; calcification in a child under about 10 years suggests a tumour.
- Germinoma (commonest pineal tumour, children and young adults, mainly males): hyperdense mass engulfing the calcification, often with a synchronous suprasellar lesion. Pineoblastoma tends to scatter calcification to the edge.
- A pineal mass compresses the tectum, causing upward gaze palsy, and the aqueduct, causing obstructive hydrocephalus.
Pituitary: development and relations
| Part | Origin | Imaging point |
|---|---|---|
| Anterior (adenohypophysis) | Rathke pouch, oral ectoderm | Enhances later than the stalk and posterior lobe |
| Posterior (neurohypophysis) | Downgrowth of the diencephalon (neuroectoderm) | T1 bright spot from stored vasopressin granules; absent in central diabetes insipidus |
- The posterior lobe has pituicytes (glia) and Herring bodies (axon swellings holding hormone). Anterior lobe basophils make FSH, LH, TSH and ACTH; acidophils make GH and prolactin.
- ADH and oxytocin are made in the supraoptic and paraventricular nuclei of the hypothalamus and only stored and released by the posterior lobe, so posterior lobe injury causes diabetes insipidus that may recover once the stalk stump releases hormone. The anterior lobe receives hypothalamic releasing hormones through the hypophyseal portal system.
- Prolactin is the only anterior hormone under mainly inhibitory control (dopamine), so stalk compression or removal of hypothalamic input raises prolactin while the others fall. Prolactinoma is the commonest functioning adenoma (galactorrhoea, amenorrhoea); somatotroph adenoma is next. Bromocriptine and cabergoline are dopamine D2 agonists that suppress prolactin and shrink the tumour.
- Sheehan syndrome: the gland enlarged by pregnancy has a fragile low-pressure portal supply, so postpartum haemorrhage and shock cause ischaemic necrosis; failure of lactation is often the first sign.
- A remnant of Rathke pouch can leave a Rathke cleft cyst (ciliated cuboidal lining, non-enhancing, between the lobes) or an ectopic adenoma in the sphenoid sinus along the craniopharyngeal canal.
- Relations: roof, diaphragma sellae (pierced by the stalk); floor, sphenoid body over the sphenoid sinus; above, optic chiasm; laterally, cavernous sinus. Tumours erode downwards into the sphenoid, and surgeons reach the gland by the transsphenoidal route through the nose and sphenoid sinus.
- Cavernous sinus: ICA and VI run inside the sinus (VI is often first hit in sinus thrombosis); in the lateral wall, from above down, lie III, IV, V1 and V2 (lowest).
- Cavernous sinus thrombosis usually follows infection of the "danger area" of the face (a furuncle on the nose or upper lip) spreading through the valveless facial and ophthalmic veins, or sphenoid sinusitis.
- Blood supply: the superior hypophyseal artery feeds the capillary plexus in the median eminence; portal veins carry releasing hormones to the anterior lobe, which has almost no direct arterial supply. So on dynamic MRI the normal gland brightens early and a microadenoma stays dark then fills in late.
Sellar and suprasellar masses
| Lesion | Imaging clue |
|---|---|
| Macroadenoma (10 mm or more) | Expands the sella; narrow waist at the diaphragma gives a snowman shape; upward growth compresses the chiasm, lateral growth the cavernous sinus nerves |
| Pituitary apoplexy | Sudden headache and ophthalmoplegia; T1 bright blood, fluid level |
| Craniopharyngioma | Child, suprasellar, cystic with calcification and enhancing rim; "machinery oil" fluid; palisading epithelium with wet keratin |
| Empty sella | Sella filled with CSF, flattened gland, midline stalk; arachnoid herniation; idiopathic intracranial hypertension |
| Lymphocytic hypophysitis | Late pregnancy or postpartum; symmetrical enlarged gland, thick midline stalk |
- Pregnancy: lactotroph hyperplasia under oestrogen makes the gland up to about 10–12 mm tall with a convex top; normal for pregnancy only.
- Visual fields: an adenoma presses the chiasm from below, giving upper bitemporal quadrant loss first; a craniopharyngioma from above gives lower quadrant loss first; both end as bitemporal hemianopia.
Remember Posterior pituitary bright on T1 because it stores hormone; anterior pituitary late to enhance because its blood arrives through portal veins.
Exam trap Lentiform nucleus means putamen plus globus pallidus; the caudate is not part of it.
Exam trap Upward growth of a pituitary mass affects the chiasm; lateral growth affects the cavernous sinus nerves (in apoplexy most often III).
How FCPS asks about this
- Thalamic nucleus relaying taste: ventral posteromedial (VPM).
- Teenager with tremor, raised liver enzymes, T2 bright putamina: Wilson disease; ATP7B copper transporter.
- Pulvinar brighter than the putamen: variant CJD.
- Commonest pineal tumour: germinoma; Parinaud upward gaze palsy.
- Lowest nerve in the cavernous sinus lateral wall: maxillary (V2); VI lies inside the sinus.
- Mechanism of bromocriptine: dopamine D2 agonist suppressing prolactin.
- Posterior hypothalamic lesion: loss of heat conservation (poikilothermia); anterior lesion causes hyperthermia.
Test yourself on this topic
5 of the 48 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
Which structures together form the corpus striatum?
Answer: Caudate and lentiform nuclei
The corpus striatum is the caudate nucleus together with the lentiform nucleus, named for the grey and white striations where bridges of grey matter cross the internal capsule. The lentiform nucleus is itself made of the putamen laterally and the globus pallidus medially. The caudate and putamen, which have the same cell structure and connections, form the striatum (neostriatum), the input part of the basal ganglia. The globus pallidus is the paleostriatum and the main output.
Corpus striatum
- Corpus striatum = caudate + lentiform
- Lentiform = putamen + globus pallidus
- Striatum = caudate + putamen
- Globus pallidus = main output
Remember Corpus striatum: caudate plus lentiform.
Exam trap Do not confuse the corpus striatum (caudate plus lentiform) with the striatum (caudate plus putamen).
Why the other options are wrong
- Putamen and globus pallidus These form the lentiform nucleus, only part of the corpus striatum.
- Thalamus and caudate nucleus The thalamus is not part of the striatum.
- Claustrum and putamen The claustrum is a separate thin sheet lateral to the putamen.
- Subthalamus and substantia nigra Functionally linked basal ganglia, but not part of the corpus striatum.
A 72-year-old woman with poorly controlled type 2 diabetes develops sudden involuntary flinging and writhing movements of her left arm and leg. Blood glucose is 27 mmol/L (486 mg/dL) without ketones. No haemorrhage or infarct is found, and the movements settle over weeks as glucose is controlled. What is the most likely cause?
Answer: Non-ketotic hyperglycaemia
Non-ketotic hyperglycaemia in elderly diabetics, often Asian women, can cause acute hemichorea-hemiballism from metabolic or microvascular injury to the contralateral striatum, with reduced GABA activity. Movements usually improve once glucose is controlled. On imaging the contralateral putamen is characteristically bright on T1 and mildly dense on CT without mass effect. Ketotic states rarely cause this, because ketones may be used as an alternative source to make GABA.
Hyperglycaemic hemichorea
- Elderly diabetic, no ketones
- Sudden contralateral chorea-ballism
- Contralateral putamen affected
- Settles with glucose control
Remember Hemichorea plus very high glucose: correct the glucose.
Exam trap Hemiballism is classically from a subthalamic lesion, but in diabetics check the glucose first.
Why the other options are wrong
- Acute putaminal haemorrhage Haemorrhage has been excluded, and it would cause hemiparesis.
- Wilson disease Gives bilateral movement disorder and liver disease in a young patient.
- Manganese deposition Seen with liver failure or welding exposure, giving parkinsonism.
- Basal ganglia calcification Usually bilateral and chronic, not acute with very high glucose.
A 4-year-old girl has bouts of inappropriate laughter that her parents describe as fits, and early breast development. A small mass hangs from the tuber cinereum between the stalk and mammillary bodies and has not grown over two years. What is the diagnosis?
Answer: Hypothalamic hamartoma
A hypothalamic hamartoma is a non-neoplastic mass of disorganised but mature neurons and glia attached to the tuber cinereum. Because it is a malformation, it does not grow. It typically causes gelastic (laughing) seizures and central precocious puberty, the latter because the hamartoma contains GnRH-secreting neurons. On MRI it matches grey matter on every sequence and does not enhance.
Hypothalamic hamartoma
- Hangs from tuber cinereum
- Mature neurons, does not grow
- Gelastic seizures
- Central precocious puberty (GnRH)
Remember Laughing fits and early puberty: hamartoma of the tuber cinereum.
Exam trap Do not mistake this stable malformation for a tumour needing urgent biopsy.
Why the other options are wrong
- Optic pathway glioma A growing tumour that involves the optic nerves or chiasm.
- Craniopharyngioma Usually cystic and calcified, often with growth failure.
- Suprasellar germinoma Grows and often causes diabetes insipidus.
- Langerhans cell histiocytosis Thickens the stalk with diabetes insipidus.
Six weeks after an uncomplicated delivery, a 29-year-old woman has headaches, fatigue, low blood pressure, low morning cortisol and new polyuria. Her pituitary is symmetrically enlarged with a thickened stalk; there was no significant bleeding at delivery. What is the most likely diagnosis?
Answer: Lymphocytic hypophysitis
Lymphocytic hypophysitis is an autoimmune inflammation of the pituitary, with dense lymphocytes and plasma cells, that typically affects women in late pregnancy or the months after delivery. The gland swells symmetrically and the stalk thickens; stalk involvement can cause diabetes insipidus. ACTH deficiency is characteristically early and can be dangerous. Sheehan syndrome needs severe postpartum haemorrhage and leaves a small gland.
Lymphocytic hypophysitis
- Late pregnancy or postpartum
- Symmetric enlargement, thick stalk
- Early ACTH deficiency
- May cause diabetes insipidus
Remember Postpartum woman, swollen gland, low cortisol, no bleed: hypophysitis.
Exam trap Immune checkpoint inhibitor drugs now cause a similar hypophysitis in cancer patients.
Why the other options are wrong
- Non-functioning macroadenoma Usually grows slowly, displaces the stalk and rarely causes diabetes insipidus.
- Sheehan syndrome Follows severe postpartum bleeding and leaves a small or empty sella.
- Prolactinoma Causes high prolactin and galactorrhoea, not early ACTH loss.
- Pituitary apoplexy Causes sudden thunderclap headache from bleeding into a tumour.
A 55-year-old man has a sudden severe headache, vomiting, double vision, bitemporal field loss and hypotension. At urgent transsphenoidal surgery, an enlarged pituitary tumour is filled with fresh blood clot and necrotic tissue. What has happened?
Answer: Haemorrhage into a pituitary adenoma
Pituitary apoplexy is sudden haemorrhage or infarction in a pituitary tumour, usually a previously unknown macroadenoma. Rapid expansion causes thunderclap headache, visual loss from chiasm compression and ophthalmoplegia from pressure on the cavernous sinus nerves. Acute loss of ACTH causes hypotension and can cause life-threatening adrenal insufficiency, so steroids are given at once. On MRI the blood gives high T1 signal, sometimes with a fluid-fluid level.
Pituitary apoplexy
- Bleed or infarct in an adenoma
- Thunderclap headache, visual loss, diplopia
- Acute ACTH loss: hypotension
- Give steroids urgently
Remember Sudden headache with a bleeding pituitary tumour: apoplexy; give steroids.
Exam trap Apoplexy can mimic subarachnoid haemorrhage; look at the sella on every thunderclap CT.
Why the other options are wrong
- Rupture of a cavernous carotid aneurysm Would bleed into the subarachnoid space, not fill a pituitary tumour.
- Formation of a pituitary abscess Develops over days with fever and pus.
- Lymphocytic hypophysitis Gives uniform inflammatory enlargement, usually around pregnancy.
- Cavernous sinus thrombosis Causes proptosis and fever without a haemorrhagic sellar mass.
Where this sits in the CPSP syllabus
- Diagnostic Radiology, Paper 2: Brain, Basal ganglia, thalamus, hypothalamus, pineal and pituitary on imaging
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