PY10.1-20 | Central Nervous System Physiology — Glossary

She appeared to be in a vegetative state — eyes open but unresponsive, no purposeful movement, no communication.

Her supplementary motor area lit up — identically to a healthy volunteer's.

Understanding sensory and motor pathways allows you to localise a lesion based on clinical signs alone, often before any imaging is done.

The physiology you learn here directly translates into the clinical skills you practise in PY10.19 and PY10.20.

From Anatomy: The spinal cord has grey matter (cell bodies) surrounded by white matter (ascending and descending tracts).

From earlier Physiology: The resting membrane potential of a neuron is approximately -70 mV.

From Biochemistry: Acetylcholine, noradrenaline, dopamine, serotonin, GABA, and glutamate are the major neurotransmitters.

The central nervous system consists of the brain (cerebrum, diencephalon, brainstem, cerebellum) and the spinal cord.

The central nervous system consists of the brain (cerebrum, diencephalon, brainstem, cerebellum) and the spinal cord.

Functionally, the PNS is divided into the somatic nervous system (voluntary, skeletal muscle) and the autonomic nervous system (involuntary, smooth muscle, cardiac muscle, glands).

Functionally, the PNS is divided into the somatic nervous system (voluntary, skeletal muscle) and the autonomic nervous system (involuntary, smooth muscle, cardiac muscle, glands).

The ANS has two divisions: the sympathetic (thoracolumbar outflow, T1-L2) and parasympathetic (craniosacral outflow, CN III, VII, IX, X + S2-S4).

The ANS has two divisions: the sympathetic (thoracolumbar outflow, T1-L2) and parasympathetic (craniosacral outflow, CN III, VII, IX, X + S2-S4).

A third division, the enteric nervous system (Meissner's and Auerbach's plexuses in the gut wall), operates semi-independently.

Neurotransmitters (PY10.3) are classified by chemical structure into several groups.

Acetylcholine (ACh) is the transmitter at all preganglionic autonomic synapses, the neuromuscular junction, and parasympathetic postganglionic endings.

Catecholamines — dopamine, noradrenaline, and adrenaline — share a common synthetic pathway: tyrosine is converted to DOPA by tyrosine hydroxylase (rate-limiting step), then to dopamine by DOPA decarboxylase, then to noradrenaline by dopamine beta-hydroxylase, and finally to.

Serotonin (5-HT) is derived from tryptophan.

GABA is the principal inhibitory transmitter of the brain (synthesised from glutamate by GAD).

Glutamate is the principal excitatory transmitter.

Glycine is the main inhibitory transmitter in the spinal cord and brainstem.

The synapse (PY10.4) is the junction between two neurons (or a neuron and an effector).

Neurotransmitters (PY10.3) are classified by chemical structure into several groups.

Electrically, they can be chemical (majority, unidirectional, synaptic delay of 0.5 ms, modifiable) or electrical (gap junctions, bidirectional, no delay, found in cardiac muscle and some brain circuits).

Spatial summation (multiple synapses firing simultaneously) and temporal summation (one synapse firing rapidly) determine whether the postsynaptic neuron fires.

Spatial summation (multiple synapses firing simultaneously) and temporal summation (one synapse firing rapidly) determine whether the postsynaptic neuron fires.

Reflexes (PY10.5) are involuntary, stereotyped responses to stimuli.

The basic unit is the reflex arc: receptor, afferent neuron, integration centre (spinal cord or brainstem), efferent neuron, and effector.

Reflexes are classified as monosynaptic (stretch reflex — only one synapse, e.g., knee jerk) or polysynaptic (withdrawal reflex — multiple interneurons).

The Golgi tendon reflex (inverse myotatic reflex) uses Ib afferents from Golgi tendon organs: when tension is excessive, the agonist is inhibited and the antagonist is facilitated — a protective mechanism against muscle tear.

The withdrawal (flexor) reflex is polysynaptic and involves crossed extension: the stimulated limb flexes (withdrawal) while the opposite limb extends (to maintain balance).

Receptors (PY10.6) are specialised structures that convert stimuli into nerve impulses (transduction).

The adequate stimulus is the form of energy to which a receptor has the lowest threshold.

Receptors encode stimulus intensity by frequency coding (stronger stimulus = higher firing rate) and population coding (stronger stimulus = more receptors recruited).

Receptors encode stimulus intensity by frequency coding (stronger stimulus = higher firing rate) and population coding (stronger stimulus = more receptors recruited).

The generator potential (or receptor potential) is a graded, non-propagating depolarisation at the receptor ending — when it reaches threshold, it triggers action potentials in the afferent nerve.

The Dorsal Column-Medial Lemniscus (DCML) Pathway carries fine touch, vibration, two-point discrimination, and conscious proprioception (position sense).

The Dorsal Column-Medial Lemniscus (DCML) Pathway carries fine touch, vibration, two-point discrimination, and conscious proprioception (position sense).

The first-order neuron has its cell body in the dorsal root ganglion (DRG).

Its central process enters the spinal cord and ascends ipsilaterally in the dorsal columns — fibres from the lower limb travel in the fasciculus gracilis (medial), while fibres from the upper limb travel in the fasciculus cuneatus (lateral).

Its central process enters the spinal cord and ascends ipsilaterally in the dorsal columns — fibres from the lower limb travel in the fasciculus gracilis (medial), while fibres from the upper limb travel in the fasciculus cuneatus (lateral).

The first-order neuron synapses in the nucleus gracilis or nucleus cuneatus in the lower medulla.

The first-order neuron synapses in the nucleus gracilis or nucleus cuneatus in the lower medulla.

The second-order neuron arises here, crosses the midline as the internal arcuate fibres (decussation of the medial lemniscus), and ascends through the brainstem as the medial lemniscus to synapse in the ventral posterolateral (VPL) nucleus of the thalamus.

The second-order neuron arises here, crosses the midline as the internal arcuate fibres (decussation of the medial lemniscus), and ascends through the brainstem as the medial lemniscus to synapse in the ventral posterolateral (VPL) nucleus of the thalamus.

The second-order neuron arises here, crosses the midline as the internal arcuate fibres (decussation of the medial lemniscus), and ascends through the brainstem as the medial lemniscus to synapse in the ventral posterolateral (VPL) nucleus of the thalamus.

The second-order neuron arises here, crosses the midline as the internal arcuate fibres (decussation of the medial lemniscus), and ascends through the brainstem as the medial lemniscus to synapse in the ventral posterolateral (VPL) nucleus of the thalamus.

The third-order neuron projects from VPL through the posterior limb of the internal capsule to the primary somatosensory cortex (postcentral gyrus, Brodmann areas 3, 1, 2).

The third-order neuron projects from VPL through the posterior limb of the internal capsule to the primary somatosensory cortex (postcentral gyrus, Brodmann areas 3, 1, 2).

Its central process enters the spinal cord and ascends ipsilaterally in the dorsal columns — fibres from the lower limb travel in the fasciculus gracilis (medial), while fibres from the upper limb travel in the fasciculus cuneatus (lateral).

The Anterolateral System (Spinothalamic Tracts) carries pain, temperature, and crude (non-discriminative) touch.

The first-order neuron (DRG) enters the spinal cord and synapses in the dorsal horn (substantia gelatinosa, Rexed laminae I, II, V).

The second-order neuron crosses the midline within one or two segments via the anterior white commissure and ascends in the anterolateral white matter.

The lateral spinothalamic tract carries pain and temperature; the anterior spinothalamic tract carries crude touch and pressure.

The lateral spinothalamic tract carries pain and temperature; the anterior spinothalamic tract carries crude touch and pressure.

Therefore, a spinal cord lesion affecting the anterolateral column causes contralateral loss of pain and temperature beginning one or two segments below the lesion.

This difference in crossing levels is the entire basis of Brown-Sequard syndrome (PY10.10).

Other ascending tracts worth knowing include the dorsal spinocerebellar tract (unconscious proprioception from the lower limb via Clarke's column, enters the cerebellum through the inferior cerebellar peduncle) and the ventral spinocerebellar tract (crosses twice, enters via the.

Other ascending tracts worth knowing include the dorsal spinocerebellar tract (unconscious proprioception from the lower limb via Clarke's column, enters the cerebellum through the inferior cerebellar peduncle) and the ventral spinocerebellar tract (crosses twice, enters via the.

The third-order neuron projects from VPL through the posterior limb of the internal capsule to the primary somatosensory cortex (postcentral gyrus, Brodmann areas 3, 1, 2).

The somatosensory association cortex (areas 5, 7) integrates this information for complex perception — recognising an object by touch (stereognosis), for example.

Types of pain. Acute pain is brief, well-localised, and serves a protective function (e.g., pulling your hand from a flame).

Fast pain (sharp, pricking) is carried by A-delta fibres (small, myelinated, conduction velocity 5-30 m/s).

Slow pain (burning, aching, throbbing) is carried by C fibres (unmyelinated, conduction velocity 0.5-2 m/s).

Pain receptors (nociceptors) are free nerve endings found in almost every tissue except the brain parenchyma itself (which is why brain surgery can be done under local anaesthesia).

Prostaglandins do not directly cause pain but sensitise nociceptors, lowering their threshold — this is why aspirin and NSAIDs (which inhibit cyclooxygenase and reduce prostaglandin synthesis) are effective analgesics.

Pain pathways. The first-order neuron (DRG) releases substance P and glutamate at its synapse in the dorsal horn (laminae I, II, V).

They respond to mechanical damage, extreme temperature, and chemical mediators released during tissue injury — bradykinin (the most potent pain-producing substance), prostaglandins, histamine, serotonin, potassium ions, and substance P.

This tract has two functional components: the neospinothalamic tract (direct to VPL thalamus, then to somatosensory cortex — mediates the discriminative aspect: where does it hurt?

how intense is it?) and the paleospinothalamic tract (projects to reticular formation, periaqueductal grey, and medial thalamic nuclei, then to the cingulate and insular cortex — mediates the affective-motivational aspect: suffering, unpleasantness).

Referred pain is pain perceived at a site distant from the actual source of pathology.

The mechanism involves convergence — visceral and somatic afferents from the same dermatome synapse on the same second-order neuron in the dorsal horn.

Gate Control Theory of Pain (Melzack and Wall, 1965) is one of the most important concepts in pain physiology.

The theory proposes that a "gate" mechanism in the substantia gelatinosa (lamina II) of the dorsal horn modulates pain transmission.

This explains why rubbing a painful area reduces pain — the touch input through A-beta fibres closes the gate.

This theory also explains the mechanism of TENS (Transcutaneous Electrical Nerve Stimulation) — electrical stimulation of A-beta fibres at the surface to close the gate and reduce pain perception.

Descending pain modulation. The brain does not passively receive pain — it actively controls it.

The periaqueductal grey (PAG) in the midbrain is the command centre.

When activated (by stress, fear, or opioid drugs), it sends signals to the nucleus raphe magnus in the medulla, which projects serotonergic fibres down to the dorsal horn, where they inhibit pain transmission.

A parallel noradrenergic pathway from the locus coeruleus does the same.

Both pathways activate enkephalin-releasing interneurons in the dorsal horn that presynaptically inhibit the primary afferent (reducing substance P release) and postsynaptically inhibit the projection neuron.

This is the endogenous opioid system — the reason soldiers in battle may not feel severe injuries until after the danger has passed.

The three families of endogenous opioids are: endorphins (from pro-opiomelanocortin, the most potent), enkephalins (met-enkephalin and leu-enkephalin, found in the dorsal horn), and dynorphins (from pro-dynorphin).

The three families of endogenous opioids are: endorphins (from pro-opiomelanocortin, the most potent), enkephalins (met-enkephalin and leu-enkephalin, found in the dorsal horn), and dynorphins (from pro-dynorphin).

The three families of endogenous opioids are: endorphins (from pro-opiomelanocortin, the most potent), enkephalins (met-enkephalin and leu-enkephalin, found in the dorsal horn), and dynorphins (from pro-dynorphin).

The corticospinal tract originates primarily from the primary motor cortex (precentral gyrus, Brodmann area 4, about 30% of fibres), the premotor cortex (area 6, about 30%), and the somatosensory cortex (areas 3,1,2 — about 40%).

The corticospinal tract originates primarily from the primary motor cortex (precentral gyrus, Brodmann area 4, about 30% of fibres), the premotor cortex (area 6, about 30%), and the somatosensory cortex (areas 3,1,2 — about 40%).

The corticospinal tract originates primarily from the primary motor cortex (precentral gyrus, Brodmann area 4, about 30% of fibres), the premotor cortex (area 6, about 30%), and the somatosensory cortex (areas 3,1,2 — about 40%).

The fibres descend through the corona radiata, converge in the posterior limb of the internal capsule (a critical bottleneck — a small stroke here causes devastating hemiplegia), descend through the crus cerebri (basis pedunculi) of the midbrain, the basis pontis, and form the.

The fibres descend through the corona radiata, converge in the posterior limb of the internal capsule (a critical bottleneck — a small stroke here causes devastating hemiplegia), descend through the crus cerebri (basis pedunculi) of the midbrain, the basis pontis, and form the.

The fibres descend through the corona radiata, converge in the posterior limb of the internal capsule (a critical bottleneck — a small stroke here causes devastating hemiplegia), descend through the crus cerebri (basis pedunculi) of the midbrain, the basis pontis, and form the.

The fibres descend through the corona radiata, converge in the posterior limb of the internal capsule (a critical bottleneck — a small stroke here causes devastating hemiplegia), descend through the crus cerebri (basis pedunculi) of the midbrain, the basis pontis, and form the.

The fibres descend through the corona radiata, converge in the posterior limb of the internal capsule (a critical bottleneck — a small stroke here causes devastating hemiplegia), descend through the crus cerebri (basis pedunculi) of the midbrain, the basis pontis, and form the.

At the junction of the medulla and spinal cord, approximately 85-90% of fibres cross (the pyramidal decussation or motor decussation) to form the lateral corticospinal tract, which descends in the lateral funiculus and controls limb muscles.

At the junction of the medulla and spinal cord, approximately 85-90% of fibres cross (the pyramidal decussation or motor decussation) to form the lateral corticospinal tract, which descends in the lateral funiculus and controls limb muscles.

At the junction of the medulla and spinal cord, approximately 85-90% of fibres cross (the pyramidal decussation or motor decussation) to form the lateral corticospinal tract, which descends in the lateral funiculus and controls limb muscles.

The remaining 10-15% descend uncrossed as the anterior corticospinal tract in the anterior funiculus; these cross segmentally near their level of termination and control axial (trunk) muscles.

The lateral corticospinal tract terminates on motor neurons and interneurons in the ventral horn (Rexed laminae VII, VIII, IX).

The final common pathway is the alpha motor neuron, whose axon exits through the ventral root to innervate skeletal muscle.

The corticobulbar tract follows a similar course but terminates on motor nuclei of cranial nerves (V, VII, IX, X, XI, XII) in the brainstem.

Most cranial nerve nuclei receive bilateral corticobulbar input — except the lower face (CN VII) and the tongue (CN XII), which receive predominantly contralateral input.

Most cranial nerve nuclei receive bilateral corticobulbar input — except the lower face (CN VII) and the tongue (CN XII), which receive predominantly contralateral input.

Most cranial nerve nuclei receive bilateral corticobulbar input — except the lower face (CN VII) and the tongue (CN XII), which receive predominantly contralateral input.

The Extrapyramidal System is a clinical term for all descending motor pathways other than the pyramidal tract.

Rubrospinal tract (from the red nucleus, crosses immediately, travels in the lateral funiculus alongside the corticospinal tract, facilitates flexor motor neurons — important in primates for gross limb movements).

Reticulospinal tracts — pontine (medial) reticulospinal (facilitates extensors, increases muscle tone, anti-gravity) and medullary (lateral) reticulospinal (inhibits extensors, decreases muscle tone).

Reticulospinal tracts — pontine (medial) reticulospinal (facilitates extensors, increases muscle tone, anti-gravity) and medullary (lateral) reticulospinal (inhibits extensors, decreases muscle tone).

Reticulospinal tracts — pontine (medial) reticulospinal (facilitates extensors, increases muscle tone, anti-gravity) and medullary (lateral) reticulospinal (inhibits extensors, decreases muscle tone).

Vestibulospinal tract (from the lateral vestibular nucleus of Deiters, powerfully facilitates extensors — the basis of decerebrate rigidity).

Tectospinal tract (from the superior colliculus, mediates reflex head turning toward visual or auditory stimuli).

UMN vs LMN Lesions — this distinction is the single most important concept in clinical neurology.

An upper motor neuron (UMN) lesion interrupts the descending pathway anywhere from the cortex to the level just above the anterior horn cell.

Signs include: spastic paralysis (increased tone due to loss of inhibitory input from the cortex, leaving the reticulospinal and vestibulospinal tracts unopposed); hyperreflexia (exaggerated deep tendon reflexes because the reflex arc is intact but freed from cortical.

Signs include: spastic paralysis (increased tone due to loss of inhibitory input from the cortex, leaving the reticulospinal and vestibulospinal tracts unopposed); hyperreflexia (exaggerated deep tendon reflexes because the reflex arc is intact but freed from cortical.

Signs include: spastic paralysis (increased tone due to loss of inhibitory input from the cortex, leaving the reticulospinal and vestibulospinal tracts unopposed); hyperreflexia (exaggerated deep tendon reflexes because the reflex arc is intact but freed from cortical.

Signs include: spastic paralysis (increased tone due to loss of inhibitory input from the cortex, leaving the reticulospinal and vestibulospinal tracts unopposed); hyperreflexia (exaggerated deep tendon reflexes because the reflex arc is intact but freed from cortical.

Signs include: spastic paralysis (increased tone due to loss of inhibitory input from the cortex, leaving the reticulospinal and vestibulospinal tracts unopposed); hyperreflexia (exaggerated deep tendon reflexes because the reflex arc is intact but freed from cortical.

A lower motor neuron (LMN) lesion damages the anterior horn cell or its axon.

Signs include: flaccid paralysis (decreased or absent tone); areflexia or hyporeflexia (the reflex arc itself is broken); negative Babinski (flexor plantar response or no response); significant muscle atrophy (denervation atrophy, visible within weeks); and fasciculations.

Signs include: flaccid paralysis (decreased or absent tone); areflexia or hyporeflexia (the reflex arc itself is broken); negative Babinski (flexor plantar response or no response); significant muscle atrophy (denervation atrophy, visible within weeks); and fasciculations.

Signs include: flaccid paralysis (decreased or absent tone); areflexia or hyporeflexia (the reflex arc itself is broken); negative Babinski (flexor plantar response or no response); significant muscle atrophy (denervation atrophy, visible within weeks); and fasciculations.

Signs include: spastic paralysis (increased tone due to loss of inhibitory input from the cortex, leaving the reticulospinal and vestibulospinal tracts unopposed); hyperreflexia (exaggerated deep tendon reflexes because the reflex arc is intact but freed from cortical.

Signs include: spastic paralysis (increased tone due to loss of inhibitory input from the cortex, leaving the reticulospinal and vestibulospinal tracts unopposed); hyperreflexia (exaggerated deep tendon reflexes because the reflex arc is intact but freed from cortical.

Spinal cord lesion syndromes (PY10.10): Complete transection causes loss of ALL motor and sensory function below the level of the lesion.

Complete transection causes loss of ALL motor and sensory function below the level of the lesion.

Initially, there is spinal shock — a period of flaccid paralysis, areflexia, and loss of autonomic function below the lesion lasting days to weeks.

Brown-Sequard syndrome (hemisection) produces the characteristic triad: ipsilateral UMN paralysis (corticospinal), ipsilateral loss of DCML (proprioception, vibration, fine touch), and contralateral loss of pain and temperature (spinothalamic) beginning 1-2 segments below the.

Central cord syndrome (e.g., syringomyelia) damages the crossing fibres of the spinothalamic tract in the anterior white commissure.

This causes bilateral loss of pain and temperature in a "cape-like" distribution (across the shoulders and upper limbs) while preserving fine touch and proprioception (DCML intact) and motor function initially.

Anterior cord syndrome (e.g., anterior spinal artery occlusion) damages everything except the dorsal columns.

Posterior cord syndrome (rare) damages only the dorsal columns: loss of proprioception and vibration with preserved motor function and pain/temperature.

Cerebellum (PY10.11) The cerebellum ("little brain") contains more neurons than the rest of the brain combined, yet it constitutes only 10% of brain volume.

Vestibulocerebellum (flocculonodular lobe) — receives input from the vestibular nuclei via the inferior cerebellar peduncle.

It controls balance and eye movements.

This is the part damaged in medulloblastoma (a childhood posterior fossa tumour).

Spinocerebellum (vermis and paravermal zone) — receives proprioceptive input from the spinal cord (spinocerebellar tracts).

Lesion: truncal ataxia (the patient sways and falls when standing, cannot walk in a straight line) and nystagmus.

Cerebrocerebellum (lateral hemispheres) — the largest part in humans.

It is involved in planning of movement, motor learning, and timing.

The output goes from the cerebellar deep nuclei (mainly the dentate nucleus) through the superior cerebellar peduncle, crosses in the midbrain, and reaches the VL nucleus of the thalamus, which projects back to the motor cortex.

The output goes from the cerebellar deep nuclei (mainly the dentate nucleus) through the superior cerebellar peduncle, crosses in the midbrain, and reaches the VL nucleus of the thalamus, which projects back to the motor cortex.

The output goes from the cerebellar deep nuclei (mainly the dentate nucleus) through the superior cerebellar peduncle, crosses in the midbrain, and reaches the VL nucleus of the thalamus, which projects back to the motor cortex.

Lesion: intention tremor (tremor that worsens as the hand approaches the target, absent at rest — the opposite of Parkinson's tremor), dysmetria (overshooting or undershooting the target, tested by finger-nose test), dysdiadochokinesia (inability to perform rapid alternating.

Lesion: intention tremor (tremor that worsens as the hand approaches the target, absent at rest — the opposite of Parkinson's tremor), dysmetria (overshooting or undershooting the target, tested by finger-nose test), dysdiadochokinesia (inability to perform rapid alternating.

Lesion: intention tremor (tremor that worsens as the hand approaches the target, absent at rest — the opposite of Parkinson's tremor), dysmetria (overshooting or undershooting the target, tested by finger-nose test), dysdiadochokinesia (inability to perform rapid alternating.

Lesion: intention tremor (tremor that worsens as the hand approaches the target, absent at rest — the opposite of Parkinson's tremor), dysmetria (overshooting or undershooting the target, tested by finger-nose test), dysdiadochokinesia (inability to perform rapid alternating.

Lesion: intention tremor (tremor that worsens as the hand approaches the target, absent at rest — the opposite of Parkinson's tremor), dysmetria (overshooting or undershooting the target, tested by finger-nose test), dysdiadochokinesia (inability to perform rapid alternating.

Basal Ganglia (PY10.12) The basal ganglia are a group of subcortical nuclei: caudate nucleus, putamen (together called the striatum — the main input structure), globus pallidus (internal segment GPi and external segment GPe — GPi is the main output), subthalamic nucleus (STN),.

The basal ganglia are a group of subcortical nuclei: caudate nucleus, putamen (together called the striatum — the main input structure), globus pallidus (internal segment GPi and external segment GPe — GPi is the main output), subthalamic nucleus (STN), and substantia nigra.

The basal ganglia are a group of subcortical nuclei: caudate nucleus, putamen (together called the striatum — the main input structure), globus pallidus (internal segment GPi and external segment GPe — GPi is the main output), subthalamic nucleus (STN), and substantia nigra.

The basal ganglia are a group of subcortical nuclei: caudate nucleus, putamen (together called the striatum — the main input structure), globus pallidus (internal segment GPi and external segment GPe — GPi is the main output), subthalamic nucleus (STN), and substantia nigra.

The basal ganglia are a group of subcortical nuclei: caudate nucleus, putamen (together called the striatum — the main input structure), globus pallidus (internal segment GPi and external segment GPe — GPi is the main output), subthalamic nucleus (STN), and substantia nigra.

The basal ganglia are a group of subcortical nuclei: caudate nucleus, putamen (together called the striatum — the main input structure), globus pallidus (internal segment GPi and external segment GPe — GPi is the main output), subthalamic nucleus (STN), and substantia nigra.

The basal ganglia are a group of subcortical nuclei: caudate nucleus, putamen (together called the striatum — the main input structure), globus pallidus (internal segment GPi and external segment GPe — GPi is the main output), subthalamic nucleus (STN), and substantia nigra.

Direct pathway (facilitates movement): Cortex excites the striatum (glutamate).

Indirect pathway (inhibits movement): Cortex excites the striatum.

Dopamine from the SNc modulates the balance: it excites D1 receptors (direct pathway — facilitating movement) and inhibits D2 receptors (indirect pathway — reducing the brake).

Parkinson's disease results from degeneration of dopaminergic neurons in the SNc.

The cardinal features are the TRAP mnemonic: Tremor (resting, pill-rolling, 4-6 Hz — disappears during voluntary movement), Rigidity (lead-pipe, or cogwheel if combined with tremor), Akinesia/Bradykinesia (slowness of movement, masked face, micrographia, shuffling gait), and.

The cardinal features are the TRAP mnemonic: Tremor (resting, pill-rolling, 4-6 Hz — disappears during voluntary movement), Rigidity (lead-pipe, or cogwheel if combined with tremor), Akinesia/Bradykinesia (slowness of movement, masked face, micrographia, shuffling gait), and.

The cardinal features are the TRAP mnemonic: Tremor (resting, pill-rolling, 4-6 Hz — disappears during voluntary movement), Rigidity (lead-pipe, or cogwheel if combined with tremor), Akinesia/Bradykinesia (slowness of movement, masked face, micrographia, shuffling gait), and.

The cardinal features are the TRAP mnemonic: Tremor (resting, pill-rolling, 4-6 Hz — disappears during voluntary movement), Rigidity (lead-pipe, or cogwheel if combined with tremor), Akinesia/Bradykinesia (slowness of movement, masked face, micrographia, shuffling gait), and.

The cardinal features are the TRAP mnemonic: Tremor (resting, pill-rolling, 4-6 Hz — disappears during voluntary movement), Rigidity (lead-pipe, or cogwheel if combined with tremor), Akinesia/Bradykinesia (slowness of movement, masked face, micrographia, shuffling gait), and.

Huntington's disease results from degeneration of the striatal neurons (especially those projecting through the indirect pathway).

The hallmark is chorea (involuntary, irregular, flowing dance-like movements).

Hemiballismus results from a lesion (usually vascular) of the subthalamic nucleus.

The basal ganglia are a group of subcortical nuclei: caudate nucleus, putamen (together called the striatum — the main input structure), globus pallidus (internal segment GPi and external segment GPe — GPi is the main output), subthalamic nucleus (STN), and substantia nigra.

Maintenance of posture and tone (PY10.13): Posture is maintained by the interplay of the vestibulospinal tract (facilitates extensors), reticulospinal tracts (pontine facilitates extensors, medullary inhibits extensors), and the corticospinal tract (facilitates flexors).

Decerebrate rigidity (extension of all four limbs) occurs when the brainstem is transected between the superior and inferior colliculi — the vestibulospinal and pontine reticulospinal tracts are intact (extensor facilitation) but the medullary reticulospinal and corticospinal.

Decorticate rigidity (flexion of upper limbs, extension of lower limbs) occurs with a lesion above the red nucleus — the rubrospinal tract (which facilitates flexors in the upper limb) is intact.

The thalamus is the relay station for virtually all sensory, motor, and limbic information reaching the cerebral cortex.

Specific relay nuclei have precise, point-to-point connections with defined cortical areas: Ventral posterolateral (VPL) nucleus — receives the medial lemniscus (DCML) and spinothalamic tract from the body.

Ventral posteromedial (VPM) nucleus — receives the trigeminothalamic tract (sensation from the face, via the trigeminal nerve) and taste fibres.

Lateral geniculate nucleus (LGN) — receives the optic tract.

Medial geniculate nucleus (MGN) — receives the inferior colliculus (auditory pathway).

Ventral lateral (VL) nucleus — receives output from the cerebellum (via the dentate nucleus and superior cerebellar peduncle) and the basal ganglia (GPi/SNr).

Ventral anterior (VA) nucleus — receives output primarily from the basal ganglia.

Anterior nucleus — part of the Papez circuit (limbic system).

Lateral dorsal (LD) and lateral posterior (LP) nuclei — association nuclei that connect with the parietal association cortex.

Non-specific nuclei have diffuse connections with wide areas of the cortex: Intralaminar nuclei (centromedian nucleus, parafascicular nucleus) — receive input from the reticular formation, spinothalamic tract, and basal ganglia.

Intralaminar nuclei (centromedian nucleus, parafascicular nucleus) — receive input from the reticular formation, spinothalamic tract, and basal ganglia.

They play a role in arousal, attention, and pain awareness.

Reticular nucleus — a thin shell of neurons surrounding the thalamus, forming a "gatekeeper" that does NOT project to the cortex.

Midline nuclei — connect with the limbic system and are involved in memory and emotion.

The pulvinar is the largest thalamic nucleus in humans.

Clinical correlates: Thalamic syndrome (Dejerine-Roussy syndrome) results from a vascular lesion (usually a stroke in the thalamogeniculate artery, a branch of the posterior cerebral artery) affecting the VPL nucleus.

Thalamic syndrome (Dejerine-Roussy syndrome) results from a vascular lesion (usually a stroke in the thalamogeniculate artery, a branch of the posterior cerebral artery) affecting the VPL nucleus.

As the lesion partially recovers, the patient develops excruciating, spontaneous, burning pain on the affected side — thalamic pain.

Thalamic lesions can also cause: contralateral hemianaesthesia (loss of all sensation), thalamic hand (abnormal posturing), and cognitive deficits if association nuclei are involved.

Hypothalamus (PY10.15) The hypothalamus is a small structure (about 4 grams, less than 1% of brain volume) that sits below the thalamus, forming the floor and lower walls of the third ventricle.

Suprachiasmatic nucleus (SCN) — the master biological clock.

Supraoptic and paraventricular nuclei — synthesise ADH (vasopressin) and oxytocin, which are transported down axons to the posterior pituitary for release into the blood.

Damage to this pathway: diabetes insipidus (dilute polyuria, up to 20 litres/day).

Arcuate nucleus — produces releasing and inhibiting hormones that control the anterior pituitary via the hypothalamo-hypophyseal portal system: GnRH, CRH, TRH, GHRH, somatostatin, dopamine (inhibits prolactin).

This nucleus also contains appetite-regulating neurons: NPY/AgRP neurons (orexigenic — stimulate appetite) and POMC/CART neurons (anorexigenic — suppress appetite).

This nucleus also contains appetite-regulating neurons: NPY/AgRP neurons (orexigenic — stimulate appetite) and POMC/CART neurons (anorexigenic — suppress appetite).

Lateral hypothalamus — the "feeding centre." Stimulation causes eating; destruction causes anorexia and starvation.

Contains orexin (hypocretin) neurons — loss of these neurons causes narcolepsy (sudden irresistible sleep attacks, cataplexy).

Ventromedial nucleus — the "satiety centre." Stimulation stops eating; destruction causes hyperphagia and obesity.

Anterior hypothalamus — controls heat loss mechanisms (vasodilation, sweating).

Posterior hypothalamus — controls heat conservation mechanisms (vasoconstriction, shivering).

Mammillary bodies — part of the Papez circuit (hippocampus to mammillary bodies via the fornix, then to the anterior thalamic nucleus via the mammillothalamic tract, then to the cingulate gyrus).

Bilateral mammillary body damage is the hallmark lesion in Wernicke's encephalopathy (thiamine deficiency, seen in chronic alcoholism — presenting with confusion, ataxia, and ophthalmoplegia).

Limbic System (PY10.15) The limbic system is a functional (not strictly anatomical) group of structures involved in emotion, motivation, memory, and autonomic regulation.

Hippocampus — critical for converting short-term memory into long-term memory (memory consolidation).

Bilateral hippocampal damage causes anterograde amnesia (inability to form new memories, while old memories are preserved).

Amygdala — the fear and emotional processing centre.

Cingulate gyrus — part of the Papez circuit, involved in emotion and pain affect.

Septal nuclei — pleasure centre.

Cerebral Cortex (PY10.16) The cerebral cortex has approximately 16 billion neurons arranged in six layers.

Primary motor cortex (area 4) — precentral gyrus.

Premotor cortex (area 6) — plans motor sequences.

Supplementary motor area (medial area 6) — bimanual coordination and internally generated movements (the area that lights up when you imagine playing tennis — as in Kate Bainbridge's case).

Broca's area (area 44, 45) — motor speech area, in the inferior frontal gyrus of the dominant hemisphere (usually left).

Damage causes Broca's aphasia (non-fluent/expressive aphasia): the patient understands speech but cannot produce fluent speech.

Primary somatosensory cortex (areas 3, 1, 2) — postcentral gyrus.

Wernicke's area (area 22) — sensory speech area, in the posterior superior temporal gyrus.

Damage causes Wernicke's aphasia (fluent/receptive aphasia): the patient speaks fluently but the speech is meaningless (word salad), and they cannot understand spoken or written language.

Arcuate fasciculus — white matter tract connecting Broca's and Wernicke's areas.

Damage causes conduction aphasia: the patient can understand and can speak fluently but cannot repeat.

Primary visual cortex (area 17) — calcarine sulcus of the occipital lobe.

Primary auditory cortex (areas 41, 42) — superior temporal gyrus.

Prefrontal cortex — executive functions: planning, decision-making, working memory, personality, social behaviour, impulse control.

Damage: personality change (the famous case of Phineas Gage, 1848 — a railroad worker who survived a tamping iron through his prefrontal cortex but underwent a dramatic personality change from responsible to impulsive and irreverent).

Cerebral dominance: In 95% of right-handed and 70% of left-handed people, the left hemisphere is dominant for language.

Cerebral dominance: In 95% of right-handed and 70% of left-handed people, the left hemisphere is dominant for language.

Reticular Activating System (RAS) The reticular formation is a diffuse network of neurons in the brainstem core, extending from the medulla through the pons to the midbrain.

The ascending reticular activating system (ARAS) is the component responsible for maintaining wakefulness and consciousness.

The ascending reticular activating system (ARAS) is the component responsible for maintaining wakefulness and consciousness.

It projects to the cerebral cortex via two routes: through the intralaminar nuclei of the thalamus (thalamocortical pathway) and directly to the cortex via the hypothalamus and basal forebrain (extrathalamic pathway).

It projects to the cerebral cortex via two routes: through the intralaminar nuclei of the thalamus (thalamocortical pathway) and directly to the cortex via the hypothalamus and basal forebrain (extrathalamic pathway).

Noradrenergic neurons in the locus coeruleus (pons) — project to the entire cortex.

Serotonergic neurons in the raphe nuclei (midline brainstem) — wide cortical projections.

Cholinergic neurons in the pedunculopontine and laterodorsal tegmental nuclei (pons) — active during waking AND REM sleep (they drive the cortical activation during dreaming).

Histaminergic neurons in the tuberomammillary nucleus (posterior hypothalamus) — promote waking.

Orexin/hypocretin neurons in the lateral hypothalamus — stabilise the switch between waking and sleeping.

A lesion of the ARAS (e.g., a brainstem stroke affecting the midbrain reticular formation) causes coma — persistent unconsciousness.

Sleep Physiology Sleep is an active, regulated process — not simply the absence of wakefulness.

Sleep architecture consists of NREM (non-rapid eye movement) sleep and REM (rapid eye movement) sleep, cycling approximately every 90 minutes through 4-6 cycles per night.

Sleep architecture consists of NREM (non-rapid eye movement) sleep and REM (rapid eye movement) sleep, cycling approximately every 90 minutes through 4-6 cycles per night.

NREM sleep has three stages (N1, N2, N3) of progressively deeper sleep: Stage N1 (5% of total sleep) — drowsiness, transition from wakefulness.

Stage N1 (5% of total sleep) — drowsiness, transition from wakefulness.

EEG shows theta waves (4-7 Hz), replacing the alpha waves of relaxed wakefulness.

Stage N2 (45-55% of total sleep) — true sleep onset.

EEG shows sleep spindles (12-14 Hz bursts generated by the thalamic reticular nucleus) and K-complexes (sharp negative wave followed by a positive component, thought to represent cortical responses to external stimuli and to prevent arousal).

EEG shows sleep spindles (12-14 Hz bursts generated by the thalamic reticular nucleus) and K-complexes (sharp negative wave followed by a positive component, thought to represent cortical responses to external stimuli and to prevent arousal).

Stage N3 (15-20% of total sleep) — slow-wave sleep (SWS) or deep sleep.

Stage N3 (15-20% of total sleep) — slow-wave sleep (SWS) or deep sleep.

EEG shows delta waves (0.5-4 Hz, high amplitude).

Active during waking, reduced during sleep, silent during REM sleep.

REM sleep (20-25% of total sleep) — also called paradoxical sleep because the EEG resembles wakefulness (low-voltage, high-frequency, desynchronised, with beta waves), yet the body is functionally paralysed.

The flip-flop switch model of sleep-wake regulation (Saper): the VLPO (ventrolateral preoptic area) of the hypothalamus is the sleep-promoting centre — it contains GABAergic and galaninergic neurons that inhibit all the wake-promoting nuclei (locus coeruleus, raphe, TMN, orexin.

The flip-flop switch model of sleep-wake regulation (Saper): the VLPO (ventrolateral preoptic area) of the hypothalamus is the sleep-promoting centre — it contains GABAergic and galaninergic neurons that inhibit all the wake-promoting nuclei (locus coeruleus, raphe, TMN, orexin.

EEG Waveforms The electroencephalogram records electrical activity of the cerebral cortex via scalp electrodes.

Beta waves (13-30 Hz) — low amplitude, desynchronised.

Alpha waves (8-13 Hz) — moderate amplitude, synchronised.

Seen during relaxed wakefulness with eyes closed, most prominent over the occipital region.

Seen during deep sleep (N3).

Memory (PY10.18) Memory is the ability to encode, store, and retrieve information.

By duration: Sensory memory (iconic for visual, echoic for auditory — lasts milliseconds to seconds, holds a brief trace of sensory input).

Short-term (working) memory — holds 7 plus or minus 2 items for about 20-30 seconds.

Long-term memory — potentially unlimited capacity and duration.

Requires consolidation, which involves the hippocampus and occurs during sleep (especially slow-wave sleep for declarative memory and REM sleep for procedural memory).

By type: Declarative (explicit) memory — consciously recalled.

Subdivided into episodic (personal events: "I ate idli for breakfast") and semantic (facts: "the mitral valve has two leaflets").

Subdivided into episodic (personal events: "I ate idli for breakfast") and semantic (facts: "the mitral valve has two leaflets").

Depends on the medial temporal lobe (hippocampus, entorhinal cortex) and is stored in association cortices.

Non-declarative (implicit/procedural) memory — unconsciously performed.

Depends on the basal ganglia, cerebellum, and amygdala — NOT the hippocampus.

The cellular basis of memory is long-term potentiation (LTP) — a sustained increase in synaptic strength following high-frequency stimulation.

Discovered in the hippocampus, LTP requires activation of NMDA receptors (glutamate receptors that are both ligand-gated and voltage-dependent — they require simultaneous presynaptic glutamate release and postsynaptic depolarisation, making them coincidence detectors).

Learning is the acquisition of new information or behaviours.

Speech (PY10.18) Speech production and comprehension involve a network of cortical areas, predominantly in the dominant (usually left) hemisphere.

Broca's area (areas 44, 45) — converts the concept of what you want to say into a motor programme for speech.

Global aphasia — damage to both Broca's and Wernicke's areas (usually a large left MCA stroke).

Transcortical aphasias — damage to areas surrounding Broca's or Wernicke's.

The vagus nerve (CN X) provides parasympathetic innervation to the thoracic and abdominal viscera down to the splenic flexure.

Neurological Examination (PY10.19, PY10.20) As a clinical skill, systematic neurological examination follows a structured sequence.

Higher mental functions include level of consciousness (Glasgow Coma Scale), orientation (time, place, person), memory (immediate, recent, remote), attention, language (fluency, comprehension, repetition, naming), and praxis.

Motor examination assesses bulk (atrophy, hypertrophy), tone (spasticity vs rigidity vs hypotonia), power (MRC grading 0-5), and coordination (finger-nose, heel-shin, rapid alternating movements).

Sensory examination tests light touch (cotton wool), pain (pinprick), temperature (cold tuning fork), vibration (128 Hz tuning fork on bony prominences), and proprioception (joint position sense).

Reflexes include deep tendon reflexes (biceps C5-6, triceps C7, knee L3-4, ankle S1-2) graded 0 to 4+, superficial reflexes (plantar response — Babinski sign), and clonus.

Cranial nerve examination (PY10.20) tests each of the twelve cranial nerves systematically: olfaction (CN I), visual acuity and fields (CN II), pupillary reflexes (CN II, III), eye movements (CN III, IV, VI), facial sensation and corneal reflex (CN V), facial expression (CN VII.

Characteristic features: non-fluent, effortful, telegraphic speech with preserved comprehension (he follows commands correctly).

Foundations (PY10.1-PY10.6): CNS = brain + spinal cord; PNS = somatic + autonomic (sympathetic + parasympathetic + enteric) Major neurotransmitters: ACh (NMJ, autonomic), glutamate (excitatory), GABA (inhibitory in brain), glycine (inhibitory in spinal cord), catecholamines.

Sensory Pathways (PY10.7, PY10.8): DCML (fine touch, proprioception, vibration): DRG to ipsilateral dorsal columns to nucleus gracilis/cuneatus to contralateral medial lemniscus to VPL thalamus to S1 cortex.

Motor Pathways (PY10.9, PY10.10): Pyramidal: cortex to posterior limb of internal capsule to crus cerebri to pyramid to decussation (85-90% cross) to lateral corticospinal tract to alpha motor neuron UMN lesion: spastic paralysis, hyperreflexia, Babinski positive, clonus, no.

Cerebellum (PY10.11): Vestibulocerebellum (flocculonodular): balance, eye movements.

Basal Ganglia (PY10.12, PY10.13): Direct pathway (D1, facilitates movement): cortex to striatum to GPi (inhibition) = thalamic disinhibition Indirect pathway (D2, inhibits movement): cortex to striatum to GPe to STN to GPi = thalamic inhibition Parkinson's (SNc dopamine.

Thalamus (PY10.14): VPL: body sensation.

Hypothalamus and Limbic System (PY10.15): Hypothalamus: temperature (anterior = cooling, posterior = heating), appetite (lateral = feeding, ventromedial = satiety), ADH/oxytocin (supraoptic/paraventricular), circadian rhythm (SCN), pituitary control (arcuate) Hippocampus:.

Cerebral Cortex (PY10.16): Motor cortex (area 4): precentral gyrus, motor homunculus Broca's (areas 44-45): non-fluent aphasia.

Sleep and EEG (PY10.17): NREM: N1 (theta), N2 (spindles, K-complexes), N3 (delta, growth hormone, restorative) REM: paradoxical sleep, dreaming, muscle atonia, EEG like waking Flip-flop switch: VLPO (sleep) vs ARAS (wake), stabilised by orexin.

Learning, Memory, Speech (PY10.18): Declarative memory: hippocampus-dependent, consolidated during SWS Procedural memory: basal ganglia + cerebellum, hippocampus-independent LTP: NMDA receptors, Ca2+ influx, AMPA receptor insertion, CREB for long-term Aphasias: Broca's.

Clinical Examination (PY10.19, PY10.20): Systematic: higher functions to motor to sensory to reflexes to cranial nerves Key UMN vs LMN signs at the bedside differentiate cortical from spinal from peripheral lesions