The Nervous System

Part 5 · Head, neck and the nervous system

Brain, spinal cord, tracts, cranial nerves, and the art of localisation

Localisation is the whole game

Neurological physiotherapy rests on one skill: taking a pattern of deficits and deducing where the lesion is. Weakness plus loss of pain and temperature on one side, with loss of proprioception on the other, is a hemisection of the cord. Weakness of the face, arm and leg on one side with the forehead spared is a lesion above the facial nucleus. Ataxia with intention tremor and dysdiadochokinesia is cerebellar, and the side of the signs tells you the side of the lesion.

None of that requires a scanner. It requires knowing where the tracts run, where they cross, and what each region does. That is what this chapter is for.

Learning outcomes

• Describe the organisation of the nervous system and the structure of the neuron and neuroglia.
• Describe the lobes of the cerebrum and their functions, including the homunculus and language areas.
• Describe the basal ganglia, thalamus, cerebellum and brainstem, and the syndromes of each.
• Describe the internal structure of the spinal cord and the major ascending and descending tracts, with their decussation levels.
• Distinguish upper from lower motor neuron lesions.
• Describe the classical spinal cord syndromes and the ASIA classification.
• Name the cranial nerves, their functions, nuclei and clinical tests.
• Describe the meninges, ventricles, CSF and the cerebral blood supply.
• Explain the vascular territories and their clinical syndromes.
• Explain neuroplasticity and its implications for rehabilitation.

Organisation and cells

Figure 1 · How the nervous system is divided

The neuron and its supporting cells

Why peripheral nerves regenerate and central axons do not: Schwann cells and the endoneurial tube provide a permissive, guiding environment with growth factors, allowing regrowth at roughly 1 mm per day. In the CNS, oligodendrocytes and the astrocytic glial scar produce inhibitory molecules (Nogo-A, MAG, chondroitin sulphate proteoglycans), and there is no equivalent guidance tube. This is the fundamental reason a peripheral nerve injury recovers and a spinal cord injury does not — and the reason CNS rehabilitation depends on plasticity and reorganisation rather than regeneration.

Fibre types (Erlanger–Gasser), because they determine what you can test and what modalities affect:

Large fibres are the first affected by compression and the last affected by ischaemia; small fibres the reverse — which is why compressive neuropathy loses vibration and light touch first while ischaemia and diabetic small-fibre neuropathy lose pain and temperature first.

The cerebrum

Figure 2 · The brain

Lobes and functions

The homunculus. Both the motor and sensory cortices are somatotopically mapped, with representation proportional to precision of control or sensory density, not to body size. The hand, face and tongue occupy disproportionately large areas; the trunk very little. Two clinical consequences:

• The lower limb representation lies on the medial surface, in the anterior cerebral artery territory, while the face and upper limb lie laterally in the middle cerebral artery territory — which is why ACA and MCA strokes produce opposite patterns of limb weakness (§23.9).
• The map is plastic, and reorganises with use, disuse, amputation and training — the neuroanatomical basis of everything in §23.10.

Arcuate fasciculus connects Wernicke’s to Broca’s area; its lesion produces conduction aphasia — fluent speech with good comprehension but impaired repetition.

Corpus callosum — the largest commissure, connecting the hemispheres.

Internal capsule — the compact white matter funnel between the basal ganglia and thalamus, carrying the corticospinal and corticobulbar fibres in the posterior limb and genu. Because everything is packed together, a small lacunar infarct here produces a dense complete contralateral hemiplegia — the classic “pure motor stroke”, disproportionate to lesion size.

Basal ganglia, thalamus and cerebellum

Basal ganglia

Caudate nucleus + putamen (= striatum), globus pallidus (= lentiform with putamen), subthalamic nucleus, substantia nigra.

Function: they do not initiate movement; they modulate it — selecting desired movement and suppressing unwanted movement, through the direct (facilitatory) and indirect (inhibitory) pathways, both modulated by dopamine from the substantia nigra pars compacta.

Basal ganglia lesions produce hypokinetic or hyperkinetic movement disorders — NOT weakness, and NOT the classical UMN signs. Rigidity is not spasticity: rigidity is velocity-independent and present in both directions; spasticity is velocity-dependent with a clasp-knife quality. Confusing the two is one of the commonest errors in neurological assessment.

Rehabilitation implication: the basal ganglia deficit is in internally generated, automatic, sequential movement. External cues bypass the deficit by routing movement through cortical–cerebellar pathways — which is precisely why auditory cueing (metronome), visual cues (floor lines), attentional strategies and large-amplitude training (LSVT BIG) work in Parkinson’s disease. That is anatomy generating a treatment.

Thalamus

The great sensory relay — all ascending sensory pathways except olfaction synapse here before reaching the cortex. Key nuclei: VPL (body sensation), VPM (face), LGB (vision), MGB (hearing), VA/VL (motor relay from basal ganglia and cerebellum).

Thalamic lesion → contralateral sensory loss and, in a proportion, Dejerine–Roussy syndrome: severe, intractable central post-stroke pain with allodynia and hyperpathia in the anaesthetic territory.

Hypothalamus — autonomic control, temperature regulation, endocrine control via the pituitary, hunger, thirst, circadian rhythm.

Cerebellum

Three functional divisions:

The cardinal rule: cerebellar signs are IPSILATERAL — because the cerebellar output decussates in the superior cerebellar peduncle and then the corticospinal tract decussates again, a double crossing that returns the influence to the same side.

Signs (DANISH): Dysdiadochokinesia, Ataxia, Nystagmus, Intention tremor, Scanning (staccato) speech, Hypotonia. Plus dysmetria (past-pointing), rebound phenomenon, and impaired heel-shin testing.

Peduncles: superior (mainly output, to the red nucleus and thalamus), middle (input from the pontine nuclei), inferior (input from the spinal cord and vestibular nuclei).

Brainstem

Mnemonic: “2 above 2, 4 in the pons, 4 in the medulla” — CN I and II are not brainstem; III and IV in the midbrain; V–VIII pontine; IX–XII medullary.

Reticular formation — running through the whole brainstem; the ascending reticular activating system governs consciousness and arousal; descending components modulate muscle tone, pain (descending inhibition) and autonomic function.

The spinal cord: internal structure and tracts

Figure 3 · Grey and white swap places

Structure

Grey matter centrally (H-shaped: dorsal, lateral and ventral horns), white matter peripherally in dorsal, lateral and ventral columns. Rexed laminae I–X organise the grey matter; laminae I, II (substantia gelatinosa) and V are the key nociceptive laminae and the site of gate control.

The lateral horn (T1–L2) contains preganglionic sympathetic neurons; S2–S4 contains the parasympathetic equivalent.

Ascending (sensory) tracts

The decussation difference is the single most useful fact in spinal cord localisation. Dorsal columns cross high, in the medulla; spinothalamic crosses low, at the level of entry. Therefore in a cord hemisection you get ipsilateral proprioceptive loss and contralateral pain and temperature loss — the dissociated sensory loss of Brown-Séquard syndrome.

Descending (motor) tracts

The reticulospinal and vestibulospinal tracts matter more in rehabilitation than their textbook billing suggests: much of the recovery of gross proximal and trunk function after corticospinal damage is mediated by these surviving pathways, and much of the tone abnormality after stroke arises from their release from cortical inhibition.

Upper versus lower motor neuron lesion

Motor neurone disease (ALS) characteristically produces mixed upper and lower motor neuron signs — brisk reflexes in a wasted, fasciculating limb — which is diagnostically distinctive.

A crucial caveat for acute practice: in the first hours to weeks after an acute UMN lesion, there is a period of SPINAL SHOCK or CEREBRAL SHOCK — flaccidity and areflexia, which resemble a lower motor neuron picture. Spasticity develops later. Judging a lesion level from tone in the first days is unreliable.

Spinal cord syndromes and SCI classification

ASIA classification

The International Standards for Neurological Classification of Spinal Cord Injury:

• Neurological level — the most caudal segment with normal sensation AND at least grade 3 motor power, with normal function above.
• AIS grades: A complete (no sacral sparing) · B sensory incomplete · C motor incomplete, more than half of key muscles below the level grade <3 · D motor incomplete, at least half grade ≥3 · E normal.
• Sacral sparing — voluntary anal contraction, deep anal pressure, or S4–S5 sensation — is what defines an incomplete injury, and it is prognostically decisive.
• 28 key sensory points and 10 key muscles per side are tested.

Autonomic dysreflexia must be flagged here because it is a physiotherapy emergency: in lesions at or above T6, a noxious stimulus below the level (typically a blocked catheter, bowel distension, pressure injury, or an ingrowing toenail) triggers unopposed sympathetic outflow → severe hypertension, pounding headache, flushing and sweating above the level, pallor below, and reflex bradycardia. Sit the patient up, loosen constrictive clothing, and find and remove the stimulus. Untreated, it causes stroke, seizure and death.

The cranial nerves

Mnemonic for names: Oh Oh Oh To Touch And Feel Very Good Velvet, Ah Heaven. For type (S = sensory, M = motor, B = both): Some Say Marry Money But My Brother Says Big Brains Matter More.

Two deviation rules that get confused constantly:

• Uvula deviates AWAY from the side of the lesion (the intact side pulls it over)
• Tongue deviates TOWARDS the side of the lesion (the intact genioglossus pushes it across)

Bulbar versus pseudobulbar palsy — a distinction with direct swallowing implications:

Meninges, ventricles and CSF

Figure 4 · The spinal cord in section, and its coverings

The meninges

Space

Contents

Haemorrhage

Extradural

Potential

Middle meningeal artery at the pterion; lucid interval, biconvex (lens) shape on CT

Subdural

Potential

Bridging veins; crescent-shaped; chronic in the elderly and alcoholic after minor trauma — often presenting weeks later with confusion or a fluctuating hemiparesis, and easily missed

Subarachnoid

CSF, major vessels

Berry aneurysm rupture — “thunderclap” worst-ever headache, neck stiffness, photophobia

Ventricles and CSF

Two lateral ventricles → interventricular foramina (of Monro) → third ventricle → cerebral aqueduct (of Sylvius) → fourth ventricle → foramina of Luschka (lateral) and Magendie (median) → subarachnoid space → arachnoid granulations → superior sagittal sinus.

CSF: ~150 mL total, produced at ~500 mL/day by the choroid plexus — so it turns over three to four times daily. Clear, with glucose ~⅔ of plasma, protein 15–45 mg/dL, and fewer than 5 cells/mm³. Functions: buoyancy (reducing the brain’s effective weight from ~1400 g to ~50 g), cushioning, and metabolic exchange.

Hydrocephalus: communicating (impaired absorption — post-haemorrhagic, post-meningitic) or non-communicating/obstructive (aqueduct stenosis, tumour). Normal pressure hydrocephalus presents with the triad of gait apraxia (“magnetic” gait), urinary incontinence and dementia — “wet, wacky and wobbly” — and is important because the gait disturbance is often the presenting complaint to a physiotherapist and it is treatable.

Blood supply and stroke syndromes

The circle of Willis

Formed by:

• anterior communicating artery joining the two anterior cerebral arteries
• the internal carotids
• the two posterior communicating arteries
• and the two posterior cerebral arteries from the basilar. It provides collateral circulation — complete and effective in only about half of people, which is why anatomical variation partly determines stroke severity

Territories and syndromes

Stroke recognition: FAST (Face, Arms, Speech, Time) for public use; BE-FAST adds Balance and Eyes, capturing posterior circulation strokes that FAST misses.

The physiotherapy imperative: thrombolysis and thrombectomy are time-critical, and very early mobilisation must be calibrated rather than maximal — the AVERT trial found that very early, high-dose out-of-bed activity within 24 hours produced worse outcomes than usual care, while shorter, more frequent sessions were favourable. The message is early and frequent, not early and aggressive.

Neuroplasticity — the basis of neurological rehabilitation

Recovery after CNS injury depends on reorganisation, not regeneration. The mechanisms:

Kleim and Jones’s ten principles of experience-dependent plasticity are the most directly usable framework in neurological rehabilitation, and they translate this anatomy into prescription:

• Use it or lose it — unused circuits degrade.
• Use it and improve it — training drives plasticity.
• Specificity — the training must resemble the target function.
• Repetition matters — meaningful change requires hundreds of repetitions, not tens.
• Intensity matters — sufficient dose is required.
• Time matters — different mechanisms operate at different stages; the early critical window (roughly the first 3 months) is when plasticity is greatest.
• Salience matters — meaningful, motivating tasks drive more change.
• Age matters — plasticity declines but persists throughout life.
• Transference — training one skill can benefit related ones.
• Interference — maladaptive plasticity (compensatory patterns, learned non-use) can block recovery.

Constraint-induced movement therapy is the clearest clinical application — it directly targets learned non-use, and produces measurable cortical map reorganisation alongside functional gain.

The uncomfortable honest point: typical clinical practice delivers a small fraction of the repetitions used in the animal and trial protocols that established these effects. Studies of stroke rehabilitation sessions routinely count tens of upper limb repetitions where the evidence base suggests several hundred. Knowing the anatomy of plasticity means knowing that dose is the variable most often underdelivered.

Where students consistently go wrong

• Getting the decussation levels wrong. Dorsal columns cross in the medulla; spinothalamic crosses at cord level.
• Forgetting spinothalamic fibres ascend 1–2 segments before crossing.
• Saying cerebellar signs are contralateral. They are ipsilateral.
• Confusing rigidity with spasticity. Rigidity is velocity-independent.
• Expecting UMN signs immediately after acute injury. Spinal shock produces flaccidity first.
• Reversing the deviation rules. Uvula away, tongue towards.
• Mixing up ACA and MCA territories. ACA = leg; MCA = face and arm.
• Forgetting Wallenberg syndrome spares motor power.
• Missing autonomic dysreflexia in a T6-or-above SCI patient with headache and hypertension.
• Under-dosing repetitions in neurological rehabilitation.

Check yourself

15 questions on this chapter. Tap one to see the answer and the reasoning.

Quick review

Further reading

Chapter 23 of 24 · Human Anatomy · Physiotherapist India Next: Chapter 24 — Spinal and Peripheral Nerves: the plexuses, dermatomes and myotomes, and nerve injury.

Reviewed by the Physiotherapist India Team. · Human Anatomy contents