Anatomy: Nervous System - Central

The central nervous system (CNS) is the body’s command network, integrating sensory input, generating movement, regulating internal physiology, and supporting cognition and behavior. Anatomically, the CNS is composed of the brain and spinal cord, protected by the skull and vertebral column, wrapped in meninges, and bathed in cerebrospinal fluid (CSF) that circulates through ventricular spaces. Understanding its structure is inseparable from understanding function, because clinical neurology relies heavily on localization: identifying where a lesion sits based on a patient’s deficits. Stroke syndromes are a classic and practical example of this structure-function relationship.

Core components of the CNS

Brain: major regions and what they do

The brain can be organized into the cerebrum, diencephalon, brainstem, and cerebellum. Each contributes distinct but highly interconnected functions.

Cerebrum (cerebral hemispheres)

The cerebrum is divided into lobes with recognizable functional specializations:

• Frontal lobe
• Primary motor cortex (precentral gyrus): voluntary movement, organized somatotopically (motor homunculus).
• Premotor and supplementary motor areas: planning and initiation of movement.
• Prefrontal cortex: executive function, decision-making, working memory, social behavior.
• Dominant hemisphere language output area (classically Broca area): speech production.

• Parietal lobe
• Primary somatosensory cortex (postcentral gyrus): touch, proprioception, pain, temperature, also somatotopically organized.
• Association cortex: spatial processing and attention, particularly in the non-dominant hemisphere.

• Temporal lobe
• Auditory cortex and auditory association areas.
• Memory-related structures in the medial temporal lobe (including hippocampal formation).
• Dominant hemisphere language comprehension area (classically Wernicke area).

• Occipital lobe
• Primary visual cortex and visual processing pathways.

Functional localization matters in practice. For example, a right parietal lesion may produce left-sided neglect, while a left frontal lesion affecting language cortex can produce nonfluent aphasia.

Diencephalon: thalamus and hypothalamus

• Thalamus is a major relay for sensory (and some motor) information to the cortex. Thalamic lesions can cause contralateral sensory loss, sometimes with altered pain perception.
• Hypothalamus regulates autonomic and endocrine function through connections with the pituitary, influencing temperature, appetite, circadian rhythms, and stress responses.

Brainstem: midbrain, pons, medulla

The brainstem contains ascending and descending tracts, cranial nerve nuclei, and centers for vital functions. It is a dense neighborhood anatomically, so small lesions can have large effects.

• Midbrain: eye movement control, arousal systems, motor pathways.
• Pons: connections to cerebellum, facial sensation and movement, hearing and balance-related nuclei.
• Medulla: cardiovascular and respiratory centers, swallowing, coughing, and key motor and sensory tract pathways.

A hallmark of brainstem lesions is “crossed findings”: cranial nerve deficits on the side of the lesion with long-tract signs (motor or sensory) on the opposite side of the body.

Cerebellum

The cerebellum coordinates movement, balance, and motor learning. It does not initiate movement but refines it. Cerebellar dysfunction commonly produces ataxia, dysmetria (overshoot/undershoot), intention tremor, and gait instability. Because cerebellar pathways largely influence the ipsilateral body, cerebellar lesions typically cause ipsilateral limb ataxia.

Spinal cord: organization and pathways

The spinal cord is segmental and organized around gray and white matter.

• Gray matter contains neuronal cell bodies.
• Dorsal (posterior) horn: sensory processing.
• Ventral (anterior) horn: lower motor neurons to skeletal muscle.
• Lateral horn (notably in thoracic levels): autonomic neurons.

• White matter contains major tracts.
• Corticospinal tracts: voluntary motor control. Lesions above the level of the anterior horn lead to upper motor neuron signs (weakness, hyperreflexia, spasticity).
• Dorsal columns: vibration, proprioception, fine touch. These ascend ipsilaterally and cross in the medulla.
• Spinothalamic tracts: pain and temperature. These cross near the spinal entry level and ascend contralaterally.

This wiring explains common clinical patterns, such as why certain spinal cord lesions produce dissociated sensory loss or why deficits may appear on different sides depending on tract crossing.

Protective coverings: meninges and clinical relevance

The CNS is surrounded by three meningeal layers:

• Dura mater: tough outer layer.
• Arachnoid mater: middle layer; the subarachnoid space below it contains CSF and major cerebral vessels.
• Pia mater: delicate layer adhering to the brain and spinal cord surface.

These layers matter clinically. Hemorrhage patterns relate to meningeal anatomy and vascular structures in and around these spaces. Inflammation of the meninges (meningitis) typically causes headache, fever, neck stiffness, and can rapidly threaten neurological function.

Ventricles and cerebrospinal fluid (CSF)

CSF cushions the brain, helps maintain chemical stability, and supports waste clearance. It circulates through the ventricular system and around the brain and spinal cord in the subarachnoid space.

Key components include:

• Lateral ventricles (within each hemisphere)
• Third ventricle (midline, associated with diencephalon)
• Cerebral aqueduct (connects third to fourth ventricle)
• Fourth ventricle (between brainstem and cerebellum)

Obstruction to flow can enlarge ventricles and raise intracranial pressure, a scenario that is clinically significant because it can compress neural tissue and disrupt perfusion.

Functional localization: how anatomy predicts symptoms

Neurological localization is often a process of matching deficits to known functional maps.

Motor and sensory cortices

The primary motor and somatosensory cortices are organized somatotopically. A lesion near the lateral cortex tends to affect face and upper limb more than leg, while a lesion near the medial surface (paracentral lobule) tends to affect the lower limb more.

Language and hemispheric dominance

In most right-handed individuals and many left-handed individuals, language function is left-hemisphere dominant. Lesions in dominant frontal language output regions lead to reduced fluency with relatively preserved comprehension, while lesions in dominant temporal-parietal comprehension regions lead to fluent but often nonsensical speech with impaired understanding.

Visual pathways

Visual deficits help localize lesions along the pathway from retina to occipital cortex. Occipital lobe lesions classically produce contralateral visual field deficits. Because visual processing is distributed and organized, careful visual field testing can be highly localizing.

Clinical correlations: stroke syndromes and localization

Stroke syndromes are among the most practical applications of CNS anatomy. Vascular territories map to predictable patterns of neurological deficit.

Cortical strokes

Cortical strokes often present with “higher” cortical signs in addition to motor or sensory deficits, such as aphasia, neglect, or visual field loss. For example:

• Dominant hemisphere cortical involvement can produce aphasia.
• Non-dominant parietal involvement can produce neglect and impaired spatial awareness.
• Occipital involvement can cause contralateral visual field deficits.

The presence of cortical signs strongly suggests a lesion in the cerebral cortex rather than in the brainstem or spinal cord.

Subcortical strokes

Lesions in deep structures such as internal capsule pathways can produce dense contralateral motor weakness because many motor fibers are compacted into a small area. A relatively small infarct can therefore cause disproportionate weakness, sometimes with limited cortical signs.

Brainstem strokes

Brainstem strokes are notable for combinations of cranial nerve deficits and long-tract findings. For example, a patient may have facial weakness, abnormal eye movements, or dysphagia on one side along with contralateral weakness or sensory loss. Because respiratory and cardiovascular centers reside in the brainstem, some lesions can be life-threatening even when anatomically small.

Cerebellar strokes

Cerebellar infarcts often produce vertigo, nausea, gait instability, limb ataxia, and nystagmus. A key clinical point is that severe headache, vomiting, and rapidly worsening balance symptoms can signal posterior fossa pathology that may compromise brainstem structures due to limited space.

Bringing it together: anatomy as a clinical tool

The central nervous system is not just a collection of structures. It is a tightly organized system where function follows anatomy. Knowledge of brain regions, spinal cord tract organization, meninges, and ventricular CSF pathways provides a framework for interpreting symptoms and localizing lesions. In clinical practice, stroke syndromes highlight this relationship vividly: sudden focal deficits often point to specific functional areas and vascular territories, turning anatomy into an essential diagnostic language.