Cerebrum (largest, “grey wrinkled cap”)
Diencephalon
Brain-stem
Cerebellum
The cerebrum itself contains three evolutionary/structural components:
Cerebral hemispheres (cortex + sub-cortical white matter)
Limbic system / rhinencephalon
Basal (sub-cortical) nuclei / basal ganglia
Functions attributed to the cerebrum: memory, emotion, consciousness, higher cognition, initiation of voluntary action, interpretation of sensation.
Cerebral cortex = thin (~2–4 mm) sheet of grey matter that completely covers the hemispheres.
Fold = gyrus (pl. gyri).
Shallow groove = sulcus (pl. sulci).
Deep groove = fissure.
Most conspicuous fissure is the longitudinal fissure, dividing right and left hemispheres in the mid-line.
Central sulcus (Rolandic fissure)
Lateral sulcus (Sylvian fissure)
Parieto-occipital sulcus
Functional asymmetry exists, although the hemispheres work as an integrated unit.
LEFT: logical, analytical, verbal → dominant for language.
RIGHT: intuitive, perceptual, spatial.
\text{~97\%} of people show left-hemisphere language dominance (including most left-handers).
Sex differences: lateralisation is less pronounced in females; females therefore have lower incidence of aphasia after unilateral (left) lesions.
Corpus callosum – largest white-matter commissure; principal inter-hemispheric bridge.
Inner white matter arranged in tracts (association, commissural, projection).
Basal (sub-cortical) nuclei embedded within white matter.
Frontal – anterior to central sulcus, superior to lateral sulcus.
Parietal – posterior to central sulcus, separated from occipital by parieto-occipital sulcus.
Temporal – inferior to lateral sulcus.
Occipital – posterior pole, small.
Insula (5th lobe) – buried deep within lateral sulcus; function still incompletely understood, but left-insular damage correlates with non-fluent speech.
Brodmann (1909) identified 52 cyto-architectonic areas; these numeric labels (e.g., 4, 17, 44) remain a standard shorthand.
Primary sensory & motor areas: first cortical recipients of thalamic sensory input or final cortical origin of descending motor commands.
Association areas: adjacent expanses that integrate, interpret or plan.
Posterior half = sensory dominant (perception).
Anterior half = motor dominant (action).
Large swathes intermingle ➔ complex behaviours (language, planning, social cognition).
Executes fine voluntary movement of contralateral skeletal muscles.
Distorted somatotopic map → motor homunculus: disproportionately large face, tongue, hand represent high dexterity demands.
Association area; programs learned, sequential motor skills (e.g., signature).
Interacts with parietal sensory association cortex, basal nuclei, thalamus.
Lesion (with primary area) ⇒ spastic paralysis, loss of patterned skills.
Long reciprocal connections to all other lobes.
Generates “executive functions”: planning, judgement, prediction, self-monitoring, inhibition.
Initiates rapid conjugate saccades & visual attention shifts.
Unilateral damage ➔ both eyes deviate toward lesion.
Motor programming of articulate speech.
Anterior part (semantic), posterior part (phonologic).
Sends commands to premotor & primary motor cortex ➔ laryngeal, pharyngeal, oral, respiratory muscles.
Lesion → non-fluent (Broca) aphasia: intact comprehension, impaired output.
Receives contralateral touch, pressure, vibration, pain, temperature, proprioception.
Somatotopic sensory homunculus; density of receptors = cortical area size (large lips, tongue, pharynx).
Integrates primary input; allows object identification by feel, spatial relationships, body schema; stores tactile memories.
Supramarginal gyrus – Area 40
Angular gyrus – Area 39
Dominant (left) lesions ⇒ anomia, alexia with agraphia, finger agnosia, acalculia, L-R disorientation.
Non-dominant lesions ⇒ visuospatial neglect, impaired selective attention.
Conscious perception of sound; bilateral representation – unilateral lesion → partial loss both ears.
Analyses harmonic & rhythmic patterns; categorises sounds as speech, music, noise.
Comprehension & formulation of language.
Lesion → fluent but meaningless speech, poor comprehension (Wernicke aphasia).
Declarative memory, learning, emotional colouring of experience.
Cortex encircling Sylvian fissure in dominant hemisphere encompassing Broca, Wernicke, angular & supramarginal gyri plus inter-connecting tracts (notably arcuate fasciculus).
Core network for language formulation, comprehension, repetition.
Receives thalamic (lateral geniculate) input.
Retinotopic; right cortex maps left visual field & vice-versa.
Lesion → homonymous visual field deficits / cortical blindness.
Interprets form, colour, movement, fixation reflexes; matches present input with stored visual memories for recognition.
Deep “5th lobe” within lateral sulcus.
Roles postulated in gustation, visceral sensation, risk prediction, articulation fluency.
Dominant-insular lesion may impair well-articulated speech.
Short U-fibres link neighbouring gyri; long fasciculi link distant lobes.
• Arcuate fasciculus (AF) – posterior temporal ⇄ frontal premotor/Broca; lesion → conduction aphasia (poor repetition).
• Uncinate fasciculus (UF) – rostral temporal ⇄ orbitofrontal / prefrontal; connects memory & emotion with decision-making; mediates reward/punishment influence.
• Inferior longitudinal fasciculus (ILF) – occipital ⇄ temporal; object recognition, visual discrimination, memory linking.
Corpus callosum – massive bridge; transfers right-ear auditory input to left language cortex, among countless bilateral exchanges.
Anterior commissure – olfactory bulbs, amygdalae, inferior/medial temporal lobes.
Posterior commissure – interconnects occipital mid-brain circuits; pupil & eye-movement reflexes.
Corticospinal (motor cortex → spinal anterior horn).
Corticobulbar (motor cortex → cranial nerve nuclei).
Corticopontine (motor cortex → pontine nuclei → cerebellum).
Thalamo-cortical sensory radiations ascend conversely.
Motor & sensory homunculi illustrate disproportionate cortical allocation (example metaphor: “grotesque little human” emphasising hands & face – correlates with speech articulation muscles).
Damage to premotor + primary motor ⇒ spastic limbs.
Left-frontal Broca lesion ⇒ clear thought but inability to articulate (non-fluent aphasia).
Right-parietal lesion ⇒ spatial neglect, attention deficit.
Female brain’s more bilateral language representation ➔ protective effect (lower aphasia incidence).
Lesion of dominant insula ⇒ dysfluent, poorly articulated speech (suggesting insular role in speech motor-planning).
Ethical/Philosophical consideration: understanding lateralisation nuances cautions against over-simplistic “left-brain/right-brain” stereotypes; also underscores sex-based neurological variability – important for equitable clinical assessment.
Language dominance: \approx97\% left hemisphere.
Brodmann mapped 52 cyto-architectonic areas.
Frontal lobe occupies \approx \tfrac{1}{3} of hemispheric surface.
Frontal lobe lesions can affect speech initiation (Broca), motor planning (premotor), executive functions (prefrontal).
Parietal lobe lesions disrupt multimodal integration needed for reading, writing, calculation (angular & supramarginal gyri).
Temporal lobe is critical for auditory comprehension (Wernicke) and memory links.
Association tracts, particularly AF, underpin repetition and fluent inter-area communication – their damage creates characteristic aphasic syndromes.
Corpus callosum ensures bilateral sensorimotor coordination and linguistic transfer.
Comprehending cortical divisions and white-matter highways allows clinicians to localise lesions, predict deficits, and plan evidence-based interventions for speech, language, and cognitive disorders.