Neuroanatomy
1. What this chapter covers, and how NEET PG actually tests it
Neuroanatomy questions in NEET PG are almost always localisation questions.
A patient has a described pattern of deficits, and you are asked where the lesion is. Nothing else about the case matters.
Localisation rests on a small number of anatomical facts, and by far the most important is where each tract crosses the midline.
A tract that has already crossed produces contralateral signs. One that has not yet crossed produces ipsilateral signs. That is the entire logic.
Blood supply supplies the second half. Strokes respect arterial territories, so knowing which artery feeds which structures converts a list of deficits into a named syndrome.
This chapter covers four areas: spinal cord tracts and cord syndromes, brainstem stroke syndromes, cerebral arterial territories, and the cerebellum and basal ganglia.
| In scope here | Deliberately out of scope |
|---|---|
| Tract decussation levels and the classic cord syndromes | Detailed cytoarchitecture and Brodmann numbering |
| Brainstem cross-sectional organisation and its stroke syndromes | EEG and neurophysiological testing |
| Arterial territories, aphasia types, internal capsule lesions | Neurosurgical operative approaches |
| Cerebellar and basal ganglia lesion patterns | Pharmacological management of movement disorders (see Pharmacology) |
2. Spinal cord tracts and cord syndromes
2.1 Three tracts, three decussation levels
Everything about cord localisation follows from one table, which is worth knowing more securely than almost anything else in neuroanatomy.
| Tract | Carries | Crosses at |
|---|---|---|
| Dorsal column (gracile, cuneate) | Fine touch, vibration, proprioception | Medulla, as internal arcuate fibres |
| Spinothalamic | Pain and temperature | The level of entry, within one or two segments, in the anterior white commissure |
| Lateral corticospinal | Voluntary motor | Medullary pyramids, above the cord |
Read the consequences off directly.
Because the dorsal columns cross in the medulla, a cord lesion damages fibres that have not yet crossed, so vibration and proprioception are lost ipsilaterally.
Because the corticospinal tract also crossed above the cord, weakness is likewise ipsilateral to a cord lesion.
Because spinothalamic fibres cross almost immediately after entering, a cord lesion damages fibres that have already crossed, so pain and temperature are lost contralaterally.
The one-to-two segment delay in crossing matters clinically. Contralateral pain and temperature loss begins a couple of levels below the lesion, which is a favourite detail in stems.
2.2 Brown-Séquard syndrome
A hemisection of the cord is simply the three rules applied together.
Ipsilateral loss of motor function below the lesion, from the corticospinal tract.
Ipsilateral loss of vibration and proprioception, from the dorsal column.
Contralateral loss of pain and temperature, beginning one or two levels below.
At the level of the lesion itself there is often an ipsilateral band of complete sensory loss and lower motor neuron weakness, since the root and grey matter at that segment are destroyed.
A patient who cannot feel a pinprick on one side but cannot feel a vibrating fork on the other has a hemisection, and nothing else needs to be considered.
2.3 Syringomyelia — why the loss is a cape
A syrinx is a fluid-filled cavity expanding within the central canal region of the cord, most often in the cervical segments, and classically associated with a Chiari I malformation.
As it expands outward, the first fibres it meets are those crossing in the anterior white commissure — the spinothalamic fibres, at the moment of their decussation.
So pain and temperature are lost bilaterally, at the affected segments only, while dorsal column sensation is preserved.
That is a dissociated sensory loss, and because cervical segments are usually involved it occupies the shoulders and upper arms in a cape distribution.
The classic history follows from it: painless burns or cuts on the hands that the patient did not notice.
With further expansion the anterior horn cells are involved, adding wasting and weakness of the small hand muscles.
2.4 Subacute combined degeneration and the anterior spinal artery
Subacute combined degeneration from vitamin B12 deficiency picks out the dorsal columns, lateral corticospinal tracts and spinocerebellar tracts.
The combination gives loss of vibration and proprioception with a sensory ataxia and a positive Romberg sign, alongside upgoing plantars and spasticity.
The mixed picture of upper motor neuron signs with absent ankle jerks is characteristic, since a coexisting peripheral neuropathy blunts the reflexes.
Anterior spinal artery syndrome is the mirror image in terms of what is spared.
The artery supplies the anterior two-thirds of the cord, so corticospinal and spinothalamic tracts infarct while the dorsal columns, supplied by the paired posterior spinal arteries, survive.
The result is paralysis with loss of pain and temperature but preserved vibration and proprioception below the lesion.
Tabes dorsalis, from tertiary syphilis, instead destroys the dorsal columns and dorsal roots, producing sensory ataxia, lightning pains and the Argyll Robertson pupil that accommodates but does not react to light.
3. The brainstem
3.1 The rule of four
The brainstem looks intimidating in cross-section but obeys a simple organising rule that makes stroke syndromes derivable.
Four midline structures beginning with M: the Motor pathway (corticospinal), the Medial lemniscus, the Medial longitudinal fasciculus, and the Motor nucleus of a cranial nerve.
Four lateral structures beginning with S: the Spinocerebellar tract, the Spinothalamic tract, the Sensory nucleus of the trigeminal nerve, and the Sympathetic tract.
A medial infarct therefore gives hemiparesis, contralateral dorsal column loss and a cranial nerve palsy. A lateral infarct gives ataxia, crossed sensory loss and Horner's syndrome.
Crucially, a lateral infarct spares the pyramid, so there is no hemiparesis. That single absence identifies the syndrome immediately.
3.2 Lateral medullary (Wallenberg) syndrome
Occlusion of the vertebral artery, or of the posterior inferior cerebellar artery, infarcts the lateral medulla.
Work through the four lateral structures and the picture assembles itself.
The spinal trigeminal nucleus gives ipsilateral loss of pain and temperature on the face.
The spinothalamic tract gives contralateral loss of pain and temperature on the body.
That crossed sensory pattern — face on one side, body on the other — is the diagnostic signature of Wallenberg's.
The descending sympathetic fibres give an ipsilateral Horner's syndrome.
The spinocerebellar tract and inferior cerebellar peduncle give ipsilateral limb ataxia.
Two further structures in the lateral medulla add the rest. The nucleus ambiguus gives dysphagia, hoarseness and a diminished gag reflex, and the vestibular nuclei give vertigo, vomiting and nystagmus.
There is no hemiparesis, because the pyramid is medial and outside the territory.
3.3 Medial medullary and midbrain syndromes
Medial medullary syndrome follows occlusion of the anterior spinal artery or a vertebral branch, and follows the four M structures.
The pyramid gives contralateral hemiparesis sparing the face. The medial lemniscus gives contralateral loss of vibration and proprioception.
The hypoglossal nucleus or nerve gives ipsilateral tongue weakness, so the protruded tongue deviates towards the lesion, since the intact genioglossus pushes it across.
Weber's syndrome is a midbrain infarct in the territory of posterior cerebral artery branches.
It damages the exiting oculomotor nerve fibres and the adjacent cerebral peduncle, giving ipsilateral CN III palsy with contralateral hemiparesis.
The general pattern is worth naming. A cranial nerve deficit on one side with long tract signs on the other localises to the brainstem, at the level of that cranial nerve's nucleus.
4. Cerebral arterial territories
4.1 Reading the homunculus
The motor and sensory homunculi are arranged with the leg on the medial surface, in the paracentral lobule, and the face and hand laterally, over the convexity.
The anterior cerebral artery supplies the medial surface, and the middle cerebral artery supplies the lateral convexity.
So the artery involved is directly readable from which body part is weakest.
Anterior cerebral artery infarction gives contralateral weakness and sensory loss of the leg more than the arm, often with urinary incontinence and abulia from frontal involvement.
Middle cerebral artery infarction gives contralateral face and arm weakness more than the leg, with the additional cortical signs below.
Posterior cerebral artery infarction involves the occipital lobe, giving a contralateral homonymous hemianopia with macular sparing, because the occipital pole also receives middle cerebral collateral supply.
4.2 Cortical signs and the aphasias
Middle cerebral artery strokes add language or spatial deficits depending on the hemisphere.
In the dominant hemisphere, usually the left, the result is aphasia.
Broca's aphasia arises from the inferior frontal gyrus. Speech is non-fluent and effortful, comprehension is preserved, and the patient is typically frustrated and aware of the deficit.
Wernicke's aphasia arises from the posterior superior temporal gyrus. Speech is fluent but meaningless, comprehension is poor, and the patient is characteristically unaware.
Conduction aphasia follows damage to the arcuate fasciculus connecting the two, giving relatively preserved fluency and comprehension but disproportionately impaired repetition.
In the non-dominant hemisphere the same territory instead produces contralateral hemispatial neglect and anosognosia.
4.3 Lacunar syndromes and the internal capsule
The internal capsule carries corticospinal, corticobulbar and thalamocortical fibres in a very small volume.
It is supplied by the lenticulostriate branches of the middle cerebral artery, which are end arteries particularly vulnerable to hypertensive lipohyalinosis.
A tiny lesion here therefore causes a dense deficit, out of proportion to its size, because the fibres are so densely packed.
The classic result is a pure motor hemiparesis affecting face, arm and leg equally, with no cortical signs — no aphasia, no neglect, no visual field defect.
The absence of cortical signs alongside a dense hemiparesis is what identifies a lacunar rather than a cortical stroke.
A pure sensory stroke, from a lacune in the ventral posterolateral thalamus, is the sensory counterpart.
4.4 The circle of Willis
The circle links the anterior and posterior circulations through the anterior and posterior communicating arteries, providing collateral flow.
Its clinical importance in the exam is aneurysms.
The anterior communicating artery is the commonest site, and its aneurysms may compress the optic chiasm, giving a bitemporal field defect.
The posterior communicating artery aneurysm classically compresses the oculomotor nerve from outside.
Because parasympathetic pupillomotor fibres run superficially in CN III, external compression affects the pupil early. A painful third nerve palsy with a dilated pupil is a surgical emergency.
An ischaemic third nerve palsy, as in diabetes, affects the core of the nerve first and characteristically spares the pupil.
5. Cerebellum and basal ganglia
5.1 Why cerebellar signs are ipsilateral
Cerebellar output crosses to the opposite side, and then the corticospinal pathway it influences crosses again.
Two crossings cancel out, so cerebellar lesions produce signs on the same side as the lesion.
That double decussation is the whole explanation, and it is worth stating explicitly because it is the one exception students expect to be contralateral.
Lesions of the vermis, the midline, disturb axial and trunk control, giving truncal ataxia and a wide-based gait, as in chronic alcohol use.
Lesions of a hemisphere disturb the ipsilateral limbs, giving intention tremor, dysmetria, dysdiadochokinesia and past-pointing.
Nystagmus, scanning dysarthria and hypotonia complete the picture.
Note that a Romberg test is negative in cerebellar disease, because the deficit is not proprioceptive — the patient is unsteady with eyes open as well.
5.2 Basal ganglia lesions
Each classic movement disorder maps to a specific nucleus, and the mapping is directly examinable.
| Structure | Lesion effect |
|---|---|
| Subthalamic nucleus | Contralateral hemiballismus — violent flinging limb movements |
| Substantia nigra pars compacta | Parkinsonism — bradykinesia, rigidity, resting tremor |
| Caudate nucleus | Chorea, as in Huntington disease, with caudate atrophy and ex vacuo ventricular dilatation |
| Putamen | Commonest site of hypertensive intracerebral haemorrhage |
Hemiballismus is worth a moment of reasoning rather than recall.
The subthalamic nucleus normally drives the indirect pathway, which suppresses unwanted movement.
Losing it removes that suppression, so movement escapes uninhibited — hence the violent, involuntary flinging on the opposite side.
Wilson disease deserves mention as the reversible cause, affecting the lentiform nucleus, with Kayser-Fleischer rings and hepatic involvement in a young patient.
Worked clinical vignettes
Q1. A man is stabbed in the back. He has weakness and loss of vibration sense in the right leg, with loss of pain and temperature sensation in the left leg beginning two segments below the injury. Where is the lesion?
Pick an option to check your answer.
Show explanation
Solution. Weakness and vibration loss are on the right, and both those tracts cross above the cord, so they indicate a right-sided cord lesion.
Pain and temperature loss is on the left because spinothalamic fibres cross at the level of entry, and the two-segment delay explains why the level starts slightly below.
That combination is a right Brown-Séquard syndrome. Answer: (a).
Q2. A 62-year-old develops sudden vertigo, hoarseness and difficulty swallowing. Examination shows loss of pain sensation on the left side of the face and the right side of the body, a left Horner's syndrome and left limb ataxia. Power is normal in all four limbs. Which artery is occluded?
Pick an option to check your answer.
Show explanation
Solution. The crossed sensory pattern — face on one side, body on the other — is the signature of lateral medullary syndrome.
Every feature fits the four lateral structures plus the nucleus ambiguus and vestibular nuclei, and normal power confirms the pyramid is spared, which places the lesion laterally.
(a) A medial medullary lesion would give contralateral hemiparesis and tongue deviation instead. Answer: (b).
Q3. A hypertensive man develops sudden dense weakness of the right face, arm and leg, all equally affected. Speech is dysarthric but language, comprehension, repetition and visual fields are entirely normal. Where is the lesion?
Pick an option to check your answer.
Show explanation
Solution. Equal involvement of face, arm and leg indicates fibres are densely packed together, which happens in the internal capsule rather than across the cortical surface.
The complete absence of cortical signs — no aphasia despite a dominant hemisphere lesion, no neglect, no field defect — confirms a lacunar rather than a cortical stroke.
Right-sided weakness localises to the left side. Answer: (b).
7. Common exam traps
- Forgetting the two-segment offset in spinothalamic loss. Contralateral pain and temperature loss begins one or two levels below the cord lesion, not exactly at it.
- Expecting contralateral cerebellar signs. Two decussations cancel, so cerebellar lesions give ipsilateral signs.
- Treating a positive Romberg as evidence of cerebellar disease. Romberg is positive in proprioceptive loss, not cerebellar disease, where the patient is unsteady with eyes open too.
- Confusing medial with lateral medullary syndrome. Absence of hemiparesis places the lesion laterally; its presence with tongue deviation places it medially.
- Getting tongue deviation backwards. The tongue deviates towards the side of a hypoglossal lesion, pushed across by the intact opposite genioglossus.
- Assuming a third nerve palsy is benign. A dilated pupil suggests external compression, classically a posterior communicating artery aneurysm; pupil sparing suggests an ischaemic cause.
- Attributing dense hemiparesis to a large cortical stroke. A tiny internal capsule lacune causes an equally dense deficit but no cortical signs.
- Mixing up the aphasias. Non-fluent with intact comprehension is Broca's; fluent with impaired comprehension is Wernicke's; isolated repetition failure is conduction aphasia.
Summary
- Localisation reduces to decussation level: dorsal columns cross in the medulla, corticospinal fibres in the pyramids, spinothalamic fibres at the level of entry.
- A cord lesion therefore gives ipsilateral motor and dorsal column loss with contralateral pain and temperature loss beginning one or two levels below.
- Brown-Séquard is exactly those three rules applied together, plus a segmental band of complete loss at the level.
- Syringomyelia expands into the crossing spinothalamic fibres, giving bilateral dissociated sensory loss in a cape distribution with preserved dorsal columns.
- Subacute combined degeneration affects dorsal columns, corticospinal and spinocerebellar tracts, producing upper motor neuron signs with absent ankle jerks.
- Anterior spinal artery syndrome infarcts the anterior two-thirds and spares vibration and proprioception; tabes dorsalis does the opposite and adds the Argyll Robertson pupil.
- The rule of four organises the brainstem: four medial M structures and four lateral S structures.
- Wallenberg's syndrome is a lateral medullary infarct with crossed sensory loss, Horner's, ataxia, dysphagia and vertigo, and no hemiparesis because the pyramid is spared.
- Medial medullary syndrome gives contralateral hemiparesis and dorsal column loss with the tongue deviating towards the lesion.
- A cranial nerve palsy on one side with long tract signs on the other localises to the brainstem at that nerve's level, as in Weber's syndrome.
- Anterior cerebral artery strokes weaken the leg more than the arm; middle cerebral strokes weaken face and arm more than the leg; posterior cerebral strokes give homonymous hemianopia with macular sparing.
- Broca's aphasia is non-fluent with intact comprehension, Wernicke's is fluent with impaired comprehension, and conduction aphasia impairs repetition selectively.
- A lacunar internal capsule stroke gives a dense pure motor hemiparesis with no cortical signs, because the fibres are densely packed and the cortex is untouched.
- A painful third nerve palsy with a dilated pupil suggests posterior communicating artery aneurysm, since pupillomotor fibres run superficially; ischaemic palsies spare the pupil.
- Cerebellar signs are ipsilateral because of double decussation, with vermis lesions causing truncal ataxia and hemisphere lesions causing limb ataxia and intention tremor.
- Basal ganglia mapping: subthalamic nucleus gives contralateral hemiballismus, substantia nigra pars compacta gives parkinsonism, caudate gives chorea, putamen is the commonest hypertensive haemorrhage site.
