Nervous System

• folding (gyri = ridges, sulci = grooves) are a way to pack more neurons into a limited skull space

• more folding = more neurons = more complex processing capacity

• Lissencephaly = "smooth brain" — normal in some small mammals, but a disease in humans (missing normal gyri/sulci).

• ~80% of the brain's neurons are in the cerebellum (heavily folded even in simpler species).

• Humans: frontal lobe is proportionally largest → associated with reasoning/rationality vs. more "impulse-driven" responses in other species.

how does folding in the brain affect complex processing capacity

1. central sulcus - groove running from the top of the brain down the lateral surface (separates frontal from parietal lobe)

2. lateral (sylvian) fissure — runs horizontally along the lower lateral surface

3. preoccipital notch — small notch on the undersurface between cerebellum and rest of brain

4. parieto-occipital sulcus — imaginary line draw straight up from the preoccipital notch (better seen on medial view); separates parietal from occipital lobe

resulting lobes:

• frontal lobe — everything anterior to central sulcus, superior to lateral fissure

• parietal lobe — between central sulcus and parieto-occipital sulcus

• occipital lobe — posterior to parieto-occipital sulcus

• temporal lobe — inferior to lateral fissure

outline the landmarks used to define the lobes

• primary motor cortex (precentral gyrus)

• premotor/planning cortex (anterior to primary motor cortex)

• frontal association cortex

what are the functional areas of the frontal lobe

• located immediately anterior to central sulcus

• contains pyrimdal cells — very large, triangular neurons that project directly down to spinal cord to activate muscles

• job = execution of movement only (not planning/refinement)

• organised as motor homonculus (body map) — somatopic organisation:

  • throat → most inferior/lateral

  • face, eyes, hand (large representation) → lateral

  • trunk, legs → medial surface

• size of cortical representation is proportional to fineness of motor control needed (hence huge hand/face area vs small trunk area)

outline the primary motor cortex (precentral gyrus)

• the “brains of the motor system” — plans movement before primary motor cortex executes it

• Broca’s area: plans motor movements for speech

  • damage → Broca’s aphasia ( = non-fluent aphasia = motor aphasia — all synonyms)

  • comprehension intact, but speech is halting/effortful, poor fluency

• front eye fields: plan eye-scanning movements (e.g. reading)

• exner’s area: plans handwriting movements

outline the premotor/planning cortex (anterior to primary motor cortex)

• large volume, functions less precisely defined

• broad roles: intelligence, personality, behaviour, mood, cognitive function

outline the frontal association cortex

• primary auditory cortex

• Wernicke’s area (secondary auditory cortex)

• arcuate fasciculus

• temporal association cortex

what are the functional areas of the temporal lobe

• buried in the lateral (Sylvian) fissure

• decomposes sound into tone and timing only (tonotopic map — high vs low pitch mapped to different regions); doesn’t interpret meaning

outline the primary auditory cortex

• surrounds primary auditory cortex

• responsible for understanding/comprehension of spoken language

• damage → Wernicke’s aphasia ( = sensory aphasia)

  • speech remains fluent but makes no sense/doesn’t answer the question asked

  • contrast directly with Broca’s aphasia (fluency differs; comprehension differs)

outline the Wernicke’s area (secondary auditory cortex)

• white matter bundle connecting Wernicke’s area → Broca’s area (arch-shaped)

• damage → conduction aphasia

  • comprehension is okay, but can’t produce an appropriate verbal response (can often still write an answer)

outline arcuate fasciculus

• broad roles:

  • memory

  • mood

  • aggression

  • intelligence

outline the temporal association cortex

Type	Area damaged	Fluency	Comprehension	Alt. names
Broca's aphasia	Broca's area	❌ Non-fluent	✅ Intact	Motor / non-fluent aphasia
Wernicke's aphasia	Wernicke's area	✅ Fluent	❌ Impaired	Sensory aphasia
Conduction aphasia	Arcuate fasciculus	✅ Fluent (can understand)	✅ Intact	Connection aphasia

aphasia comparison table

• postcentral gyrus — primary somatosensory cortex (immediately posterior to central sulcus)

• supramarginal gyrus and angular gyrus (together = SMAGLA/AGLA on diagram; part of inferior partietal lobule)

• parietal association cortex

what are the functional areas of the parietal lobe

• receives sensory input: pain, temperature, discriminative touch (2-point discrimination), and proprioception (limb position sense)

• also organised as a sensory homunculus — mirrors the motor homunculus layout

outline the role of the postcentral gyrus

• support reading and writing

• rough rule of thumb: supramarginal gyrus = more reading-related, angular gyrus = more writing-related, but overlap exists

outline the supramarginal gyrus and angular gyrus

• spatial skills, 3D recognition (shapes, faces, concepts, abstract perception)

outline the role of the parietal association cortex

• primary visual cortex located at the occipital pole (seen on medial view around the calcarine sulcus)

outline the role of the occipital lobe

• non-verbal language (body language)

• emotional expression/tone of language

• spatial skills (3D)

• conceptual understanding

• artistic/musical skills

outline the role of the non-dominant (right) hemisphere of the brain

• loss of non-verbal language

• speech lacks emotion (flat prosody)

• spatial disorientation

• inability to recognise familiar objects

• loss of musical appreciation

what are the effects of injury to the right hemisphere of the brain

• primary visual cortex — at the very back of the brain (occipital pole/occipital protuberance)

• secondary visual cortex — the rest of the occipital lobe; extends down into the inferior/bottom part of the temporal lobe

what makes up the occipital lobe

• receives raw visual field input: right visual field → left hemisphere; left visual field → right hemisphere (info from both eyes crosses over)

• organised as a visuotopic map of the visual field

• extremely densely packed with neurons (huge amount of raw visual data to process)

• only organises incoming information — does NOT interpret or add meaning to it

outline the role of the primary visual cortex

• job = interpretation of what the primary visual cortex has organised (adds meaning — “what am I actually looking at”)

• takes up far more cortical territory than the primary visual cortex → reflects how much more complex interpretation is than raw data collection

• because it works from a learned model of "what normal looks like," it can be tricked — this is why magic tricks and acrobatics (e.g. Cirque du Soleil) feel so compelling: secondary visual cortex flags them as defying its expectations

• primary visual cortex itself is very rarely "wrong" — the trickery happens at the interpretation stage

outline the role of the secondary visual cortex

• cingulate gyrus — first major gyrus encountered on the medial surface

• corpus callosum — large bundle of white matter connecting the left and right hemispheres

• cerebellum — sits at the back, underneath the cerebrum

• brainstem — made up of three parts

  • midbrain

  • pons

  • medulla

what new structures can be seen in the medial view of the brain

acts as a pathway that carries information from deep brain structures back out to the cortex so it can be acted on

outline the role of the cingulate gyrus

• unique to higher primates (most other species don’t have one)

• enables left-right coordination between hemispheres

outline the role of the corpus callosum

• sits at the back, underneath the cerebrum

• coordinates movement, balance, and posture

outline the role of the cerebellum

• forebrain → cerebral cortex

• midbrain → midbrain (stays small)

• hindbrain → cerebellum + pons + medulla

outline the adult mapping of the three parts of the brain stem

Region	# of nerve pairs	Notes
Cervical	8	"Cervical" = narrowing (neck). 8 nerve pairs despite only 7 cervical vertebrae.
Thoracic	12	One pair per thoracic vertebra.
Lumbar	5	Spinal cord itself ends around vertebral level L1 — these nerves travel further down before exiting.
Sacral	5	Individual nerve roots, not true spinal cord.
Coccygeal	1	Single nerve at the very bottom.
Total	31 pairs	8 + 12 + 5 + 5 + 1

outline the sagittal view

• thickens at two points where extra limb innervation is needed

• cervical enlargement — accommodates the large number of nerves serving the upper limbs

• lumbar (thoracolumbar) enlargement — accommodates nerves serving the lower limbs

why does the spinal cord thicken at two points

• Conus medullaris — the cone-shaped tapering point where the spinal cord proper ends (~level of L1)

• Cauda equina ("horse's tail") — bundle of lumbar, sacral, and coccygeal nerve roots that continue down inside the vertebral canal after the cord has ended, before exiting at their respective vertebral levels (nicknamed "spaghetti fibres")

• Filum terminale — a thread of pia mater extending from the tip of the conus medullaris down to anchor at the coccyx

  • Function: anchors the cord so it doesn't get painfully stretched every time you bend forward and back

  • Clinical note: rugby players can tear this structure — described as extremely painful; can be surgically reanchored

outline the end of the spinal cord

from innermost (closed to cord) to outermost:

Layer	Latin meaning	Key feature
Pia mater	"soft mother"	Closely adhered directly to the spinal cord/brain surface — very hard to separate
Arachnoid mater	"spider mother"	Named for its shimmering, spider-web-like appearance
Dura mater	"tough mother"	Outermost, very tough — difficult to cut even with a scalpel

• meningitis = inflammation of these three layers

outline the meninges (the 3 protective layers)

• Dorsal rootlets (back) + ventral rootlets (front) emerge along the cord → converge into a dorsal root and ventral root

• Dorsal root + ventral root → one spinal nerve (per side, per level)

outline the anatomy at the single spinal segmental level

• Dermatome = a map of the skin showing which spinal nerve level supplies sensation to each patch of skin (e.g. the thumb is supplied by C6, the pinky by C8)

• Myotome = the equivalent map, but for muscles (motor output) rather than skin sensation

Clinical use: if someone comes in saying "I've lost feeling in my hand," you can use the dermatome map and test sensation systematically (e.g. with a pin or Q-tip) across the C6 → C7 → C8 regions of the hand/arm to work out exactly which spinal nerve level is likely affected (e.g. a pinched nerve in the spine).

outline dermatones and myotomes

• receptors: Meissner’s corpuscles and Pacinian corpuscles — these sit just beneath the skin surface and are “encapsulated” (wrapped in their own structure)

• fibre type: heavily myelinated (insulated) → fast conduction, roughly 50 metres/second

• why so fast: these receptors are firing almost constantly — clothing touching your skin, everyday bumps and pressure — so it’s worth the body’s metabolic cost of building all that myelination insulation

• route: receptor in skin → nerve fibre → cell body in dorsal root ganglion → enters the spinal cord via the dorsal root

outline the sensory pathway of discriminative touch and pressure

• receptors: free nerve endings — unencapsulated, bare nerve endings in the skin

• fibre type: unmyelinated → slow connection, roughly 1 metre/second

• why so slow: real pain is felt relatively rarely for most people (often days apart), so it isn’t “worth” the expensive cost of myelinating these fibres

• route: receptor in skin → nerve fibre → cell body in dorsal root ganglion → enters via the dorsal root → terminates directly in the back (posterior) part of the spinal cords’s grey matter

outline the sensory pathway of pain and temperature

	Touch & pressure (discriminative)	Pain & temperature (non-discriminative)
Receptor	Meissner's / Pacinian corpuscles (encapsulated)	Free nerve endings (bare)
Myelination	Heavy	None
Conduction speed	~50 m/s	~1 m/s
How often it's firing	Constantly	Rarely

• both use pseudounipolar neurons — one single process leaves the cell body (which sits in the dorsal root ganglion) and splits into two branches: one running out to the receptor in the skin, and one running central into the spinal cord (“Ganglion” just means a cluster of nerve cell bodies grouped together)

compare the similarities and differences between discriminative and non-discriminative sensory pathways

• dense clusters of cell bodies

• located inside in the centre of the cord, outside (cortex) in the brain

what is grey matter and where is it located

• the fibres/axons carrying information from A to B

• located around the outside in the spinal cord, inside in the brain

what is white matter and where is it located

• a funiculus — a large bundle/cable of white matter

• there are three major ones per side of the spinal cord

Funiculus	Location	Job / carries
Dorsal funiculus	Back of cord	Discriminative sensation (touch & pressure)
Ventral funiculus	Front of cord	Pain & temperature
Lateral funiculus	Side of cord	Motor columns

outline the three funiculi

• gracile fasciculus — medial (closer to the midline) → carries info from the lower limb (leg, thigh, foot)

• cuneate fasciculus — lateral (further from midline) → carries info from the upper limb/trunk (arm, hand, fingers)

outline the division of the dorsal funiculus and its roles

Zone	Location	Function
Substantia gelatinosa	Very back (tip of dorsal horn)	Jelly-like, unmyelinated — first stop for pain & temperature fibres
Nucleus proprius	Just in front of substantia gelatinosa	Involved in proprioception — limb position sense
(middle section — not named)	Central grey matter	Autonomic functions (e.g. balance) — not examined in detail
Lower motor neuron (LMN) pool	Front (anterior horn)	Where lower motor neurons connect to upper motor neurons to produce movement

outline the location and role of each key zone of grey matter

1. go straight up the cord in the gracile/cuneate fasciculus, or

2. detour briefly through the nucleus proprius, then rejoin the others heading up anyway

what are the two pathways a touch/pressure fibre coming in from the periphery can take

Imagine your entire forearm rests flat on a table. Thousands of receptors are all reporting essentially the same information at once. Sending every single one of those thousands of fibres all the way to the brain would need a spinal cord many times its actual size.

Instead, the nucleus proprius lets many similar fibres converge onto fewer neurons before they head upward — saving space and energy, and keeping the cord as small as it actually is (about the width of your pinky finger!).

why does touch info detour through the nucleus proprius

• reflex — encapsulated receptor sends sensory fibre directly to the LMN (lower motor neuron) pool at the same spinal level, skipping the brain entirely

• myotactic (monosynaptic) reflex — one synpase, very fast

  • e.g. knee-jerk test

• withdrawal (polysynaptic) reflex — two synapses, involves the slower pain pathway

  • example: yanking your hand back from something hot

  • uses unmyelinated pain fibres and an extra synapse, therefore slower than the myotactic reflex

outline reflexes/reflex arc

1. cell body in dorsal root ganglion

2. enters dorsal root, synapses immediately in substantia gelatinosa

3. decussates immediately, right there at the spinal level, via the ventral (anterior) white commissure

4. travels up the opposite side as the sphinothalamic tract, in the ventral funiculus

5. synapses in the thalamus

6. travels up to the primary somatosensory cortex

• key difference from DMCL: decussates immediately at the spinal cord level, not up in the medulla

outline the pain/temperature fibre pathway (sphinothalmic tract) — unmyelinated free nerve endings

1. cell body in dorsal root ganglion

2. travels up, same side, in gracile/cuneate fasciculus

3. synapses in the gracile/cuneate nucleus — in the lower medulla

4. decussates (crosses sides) via the internal acruate fibres

5. now called the medial lemniscus

6. synapses in the thalamus

7. travels via the internal capsule → primary somatosensory cortex

outline the touch and pressure fibre pathway (DCML system)

• acts as a gatekeeper

• constantly triages all incoming sensory information and decides moment to moment what’s important enough to actually pass onto the cortex

  • Example: a minor cut hurting less once a bigger pain occurs elsewhere — the thalamus has re-prioritised.

what is the role of the thalamus

	Discriminative (DCML)	Non-discriminative (Spinothalamic)
Myelination	Heavily myelinated	Unmyelinated
Conduction speed	~50 m/s	~1 m/s
Function	Touch & pressure	Pain & temperature
1st neuron terminates	Gracile/cuneate nucleus (lower medulla)	Substantia gelatinosa (spinal cord)
Decussates	Internal arcuate fibres, in the medulla	Ventral/anterior white commissure, at the spinal cord level
Named white matter tract after crossing	Medial lemniscus	Spinothalamic tract
Final relay before cortex	Thalamus	Thalamus
Destination	Primary somatosensory cortex	Primary somatosensory cortex

Discriminative vs Non-discriminative sensory pathways

• both discriminative and pain/temperature fibres from the same original (opposite) side have already crossed over by this point

  • a lesion here → loss of both touch/pressure and pain/temperature on the same side (opposite to the lesion)

• this is called an associated sensory loss (both modalities lost together, same side)

outline the affects of lesions in the brain/brainstem

• discriminative (touch/pressure) fibres haven’t crossed yet at this level → loss occurs on the same side as the lesion

• pain/temperature fibres already crossed at the spinal level → loss occurs on the opposite side to the lesion

• this is called a dissociated sensory loss (the two modalities are lost on different sides)

outline the affects of lesions in the spinal cord

Lesion location	Touch/pressure loss side	Pain/temp loss side	Type
Brain/brainstem	Opposite to lesion	Opposite to lesion	Associated
Spinal cord	Same side as lesion	Opposite to lesion	Dissociated

lesion summary table

• located in the primary motor cortex, arranged as the motor homunculus

• cell body shape: pyrimdal (triangular) — hence also called pyramidal neurons, or Betz cells

• huge compared to a typical neuron: up to ~160 micrometres wide

outline the location and structure of upper motor neurons

• they have to carry an electrical signal an extremely long way — up to 1.2 metres, from the cortex down to as low as vertebral level

• carrying a signal that far without it fading out requires a much bigger “battery” (capacitance), and that means a bigger cell

why are upper motor neurons so large

1. cell body in primary motor cortex, in the arm region of the homunculus

2. travels down through the internal capsule (completely bypasses the thalamus)

3. into the mid-brain, in an anterior (front) position — motor info always run toward the front

4. into the pons — here it temporarily breaks into many small bundles, weaving around the pons’ many nuclei, before regathering further down

5. into the lower medulla — the pyramidal decussation: ~85% of fibres cross to the opposite side here

6. after crossing, becomes the lateral corticospinal tract (in the lateral funiculus)

7. the remaining ~15% don’t cross here — they continue down the same side as the anterior corticospinal tract

8. at the relevant spinal segmental level (e.g. C5-C8 for the arm), the UMN terminates in the LMN pool (anterior/ventral horn grey matter)

9. lower motor neuron (LMN) — the second neuron — sends its fibre out through the ventral root to the muscle, causing contraction

   
   

outline the route a fibre takes down the pyramidal tract

• 15% (anterior corticospinal tract) → controls axial/trunk muscles — coarse, bulk movements (e.g. bending over to pick something up)

• 85% (lateral corticospinal tract) → controls fine manual dexterity (e.g. precise hand/finger movement)

• Key insight: fine, precise movement requires a disproportionately larger share of neural resources than coarse trunk movement — small accurate movements are neurally "expensive."

why do 85% of fibres in the pyrimdal tract cross over but 15% don’t

• About half the homunculus represents the face/head — but the face is above where the spinal cord starts, so it doesn't need spinal nerves

• Instead, a side-branch called the corticobulbar tract carries this information out to the face

• This is why the pons has a bulge on its front surface — extra nuclei needed to handle all this facial motor information

outline the corticobulbar tract

Neuron	Location	Path
1st (Upper motor neuron)	Primary motor cortex	Internal capsule → midbrain (anterior) → pons (scatters and regathers) → pyramidal decussation (lower medulla, ~85% cross) → lateral or anterior corticospinal tract → terminates in LMN pool
2nd (Lower motor neuron)	LMN pool (anterior/ventral horn)	Exits via ventral root → muscle

upper and lower motor neuron summary table

	UMN lesion	LMN lesion
Result	Spastic paralysis (spasticity / hypertonia — increased tone)	Flaccid paralysis (hypotonia — no tone)
Why	Loss of central inhibition → local reflex loop runs unchecked → muscle tone increases	No nervous input reaches the muscle at all
What you'd see	Arms held close to body (resting flexor tone); exaggerated knee-jerk reflex; resisted arm movement "overshoots" when released (person almost hits themselves)	Limb is limp when picked up and released — no resistance, no tone at all
Bedside test	Ask patient to resist you pulling their arm, then let go — exaggerated overshoot = UMN lesion	Pick up hand, let go — completely limp = LMN lesion

UMN vs LMN lesion comparison table

• caudate nucleus + putamen — together called the striatum

• globus pallidus — split into an external segment (GPe) and internal segment (GPi)

• subthalamic nucleus — sits directly beneath the thalamus

• substantia nigra — “black substance”, produces almost all of the brain’s dopamine

what five nuclei make up the basal ganglia

1. planning cortex (e.g. Broca’s area) → releases glutamate (excitatory) → activates the striatum

2. from the striatum, GABAergic (inhibitory) neurons branch three ways: to GPe, to GPi, and to the substantia nigra

   • striatum → GPi directly: uses GABA (inhibitory)

3. GPi → thalamus: uses GABA (inhibitory)

4. thalamus → planning cortex (back to where we started): uses glutamate (excitatory) — completing the loop

outline the direct pathway

1. planning cortex (e.g. Broca’s area) → releases glutamate (excitatory) → activates the striatum

2. from the striatum, GABAergic (inhibitory) neurons branch three ways: to GPe, to GPi, and to the substantia nigra

   • indirect pathway (striatum → GPe → subthalamic nucleus → GPi)

3. striatum → GPe: uses GABA (inhibitory)

4. GPE → subthalamic nucleus: uses GABA (inhibitory)

5. subthalamic nucleus → GPi: uses glutamate (excitatory)

6. GPi → thalamus: uses GABA (inhibitory)

7. thalamus → planning cortex (back to where we started): uses glutamate (excitatory) — completing the loop

outline the indirect pathway

• direct pathway — more “conservative”, models what happens if the movement is under-done

• indirect pathway — more “liberal” — models what happens if the movement is over-done (exaggerated)

• the circuit effectively averages these two scenarios and sends the result via GPi → thalamus → back to the cortex, giving the planning cortex a refined sense of the right amount of movement

• once refined, the planning cortex activates the primary motor cortex (UMN) → corticospinal tract → LMN → muscle

what do the direct and indirect pathways do

• comes from the substantia nigra

• primes the three GABAeric striatal output neurons (to GPe, GPi, and substantia nigra) so they’re ready to fire at the slightly excitatory input

• analogy: a cup filled right to the brim — it only takes the smallest additional drop (glutamate) to make it overflow (fire)

what is the role of dopamine in the basal ganglia

• the cerebellum feeds into the same glutamateric neuron that runs back up to the cortex, and does three jobs:

  1. helps orient the head for visual focus/balance

  2. general balance maintenance

  3. holds a map of what the planned movement should look like, and compares it to what’s actually happening, if they don’t match, the cerebellum sends a stop signal, letting the basal ganglia re-plan and try again

outline the role of the cerebellum in the direct and indirect pathway

• pathology: substantia nigra neurons die off (cause unclear, but linked to toxic protein accumulation) → dopamine depletion

• consequence, traced through the circuit:

  1. without dopamine “priming”, the three GABAergic striatal neurons are no longer ready to fire — much more glutamate is now needed to activate them

  2. because they’re under-activated, less inhibition reaches the GPi

  3. less inhibition on GPi → GPi neurons fire more (an inhibitory fibre that isn’t itself inhibited works harder)

  4. more GABA released from GPi → thalamus is inhibited more than normal

  5. thalamus sends less glutamate up to the cortex → hypo-excitability of the motor cortex → reduced movement (hypokinesia)

outline how Parkinson’s Disease occurs

• Rigidity — increased tone (sitting stiffly, arms/abdomen taut)

• Bradykinesia/hypokinesia — slowness, difficulty initiating movement (e.g. struggling to stand up from a chair, shuffling "freeze-then-go" gait)

• Tremor at rest

• Flat/reduced mood expression

what are the symptoms of Parkinson’s Disease