Neuroanatomy Summary

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🖋️ Notes: NEUROANATOMY NUCLEI SUMMARY

Don’t know your aunts from your peduncles? Your feta from your olives?  This page is for you.Best viewed on big screens

Waffle Warning !

You may not need to know all the locations or exact 3D structure of every one of the nuclei here, some diagrams are just to help you better picture stuff

Cerebrum

The cerebrum is the main bit you think of when you think of the brain.

Made of lots of:

-Sulcus : ridges

-Gyrus: the big bits of grey matter

Bit of Cerebrum

Location

Function

Connections & Neurotransmitters

Pathologies

Post-Central Gyrus S1

Posterior to the central sulcus

Somatosensory processing area – S1

  • Like most of the cerebrum (cortex), S1 is made up of 6 layers 
  • Just like the motor cortex, the somatosensory gyrus remembers where certain sensations came from – this is called a receptive field map
  • The receptive field map is divided into 4 areas which go from tiny (point on a finger) to big (both hands)

INPUT:  TRACTS VIA VP NUCLEUS OF THALAMUS

Several tracts. These first go to the ventral posterior (VP) nucleus of the thalamus and then go to S1 via reciprocal connections.

e.g.

  • DCMLT – dorsal column medial lemniscus – conscious proprioception 
  • Spinothalamic tract – nociception
  • Trigeminal touch pathway – column pathway for the face. Fibres project to trigeminal principal sensory nucleus, cross at the midline

-MCA stroke – contralateral loss of sensory info

Precentral Gyrus M1

Anterior to central sulcus

Makes up the M1 motor cortex

INPUT:  

Pontocerebellum (lateral bits of cerebellum) –> dentate nucleus in cerebellum via the Ventrolateral thalamus:

OUTPUT: Corticospinal tracts – cross at pyramids = contralateral

–> Contralateral movement from the M1 (but ipsilateral if you trace all the way to the cerebellum). – Audio explanation below: 

-MCA stroke:

-can’t move opposite side of body. The MCA affects face most = conttralateral hemiplegia of face

Brodmann Area 6

Just anterior to the M1 precentral gyrus

Assists in motor control

-divided into supplementary motor area 

-premotor area

INPUTS:

-Lateral parts of cerebellum (Pontocerebellum) –> dentate nucleus (DCN) –> Ventral Anterior  Thalamus –> Area 6

-MCA stroke

Parietal Lobe

Non-Dominant side (usually right hemisphere):

Spatial reasoning

  • Right parietal lobe is also responsible for body image. Lesion = you dont recognise your own hand as yours! 
  • Constructional ability–  Make stuff. Lesion = cannot put 3 -piece jigsaw puzzle together
  • Lesions in R lobe can also lead to hemineglect – you brain just doesn’t see one side of the world as being there – spoooky! 

This makes patients draw stuff like this:

Connections & Neurotransmitters

-MCA stroke

Broca's area

Dominant frontal lobe (shown in orange)

Motor speech ara at dominant side

Connected to the wernick’es area by fibres called the  arcuate fasiculus

🩸 Supplied by superior division of MCA

MCA Stroke in Broca’s area = expressive  aphasia:

-speech is very reduced with limited vocab

-very hard to make out proper sounds- speech is very jumbled

Werncike's Area

Dominant (usually left) temporal lobe

Language area of speech – chooses the correct words to say etc

Connected to the Broca’s area by fibres called the  arcuate fasiculus

Also connected to auditory cortex to help understand sounds

🩸 Supplied by inferior division of MCA

MCA Stroke in Wernicke’s area = fluent/receptive  aphasia:

-Words come out and can be heard but they don’t make any sense

-Words are random like a word salad.

-Also patient may struggle to understand words – poor comprehension 🙁 

Arcuate Fasiculus

Parietal lobule

Connects both the speech areas: Broca’s (anterior) and Wernicke’s (temporal lobe)

Connects Broca’s & Wernicke’s area together

🩸 Supplied by inferior division of MCA

Can understand and speak well BUT difficulty in repeating words 

=CONDUCTION APHASIA

Visual Cortex AKA V1

Occipital lobe at the back – Brodmann area 17

Processes most of vision from the contralateral visual field

Connected to other parts of the brain 

–> Goes up to parietal lobe for the WHERE? info

–> Goes across to temporal lobe for the WHAT lobe e.g. extrastriate body area & Fusiform Face Area

Receives info from reciprocal connections from Lateral Geniculate Nucleus LGN 

🩸 Supplied by PCA

-PCA Stroke (below is a LEFT sided pca stroke – remember brain scans are always flipped)

PCA stroke causes contralateral homonymous hemianopia (lost opposite to stroke half the visual field in both eyes ) WITH macular sparing

  • Macula has its own supply from the ophthalmic artery (branch of ICA)

PCA stroke may also affect CNIII (oculomotor) – Weber’s Syndrome – Ipsilateral enlarged pupil and ptosis, down and out gaze –  so recti don’t work and overpowered by SO & LR

Fusiform Gyrus

Medial temporal lobe

Conains fusiform face area FFA which recgonises people’s faces

Connected to V1 (area 17)

🩸 Supplied by PCA

-PCA Stroke / lesion can cause problems in recognising faces – prosopagnosia 

 

Basal Ganglia

The basal ganglia are a collection of neurones at the bottom of the brain that fine tune movement.

The basal ganglia has two pathways for movement - the direct and indirect pathways. These can be modulated by dopamine. See below:

Basal Ganglia Pathologies:

Pathology

Symptoms

Nuclei affected

Pathophysiology 

Treatment

Parkinson's Disease

  • Hypokinetic (low movement)
  • Shuffling gait (hard to walk smoothly)
  • Difficulty initiating movement
  • Fingers moving at rest: pill rolling tremor (due to lack of fluid movement)
  • Masked facial expressions
  • Cogwheel rigidity: limbs/fingers move back and forth a bit like a cog turning

Degeneration of

Substantia Nigra – SN   (produces dopamine) 

  • Dopamine leads to more movement in both pathways
  • Often, mutations in the SNCA gene lead to the alpha-synuclein protein to misfold and become sticky
  • These naughty proteins can aggregate into evil blobs called Lewy bodies 
  • Lewy bodies accumulate in SN & damage SN 
  • =LESS DOPAMINE PRODUCED

therefore lack of dopamine = less movement & problems initiating movement

-Direct pathway less active

-Indirect pathway more active

🩸Parkinsonism may also be due to strokes to areas that supply SN

-e..g paramedian branch of basilar artery (causes Weber’s Syndrome)

contralateral parkinsonism (basal ganglia supply the motor area, then the fibres cross over)

As the problem is lack of dopamine, the main treatment is to give L-DOPA, a precursor to dopamine

  • It is able to cross the Blood Brain Barrier (BBB)
  • 😊 Converted by DOPA decarboxylase from L-DOPA –> Dopamine 

Side effects of dopamine (L-DOPA) therapy:

🩸 The enzyme  Dopamine B  hydroxylase turns dopamine into NA. This can displace NA from from neurones –> can lead to HYPOTENSION (low bp)

🍼 Also can reduce prolaction  (lactating is normally kept under brakes by dopamine. Giving more dopamine can reduce breast milk flow )
🧠 May also cause psychosis
🤢 L DOPA can act in periperal chemoreceptors and cause nausea

L-DOPA can  act on peripheral dopamine receptors and cause nausea. There are two drugs (one works outside the brain – carbidopa, one inside the brain – domperidone) we can use to stop the effects of nausea:

  • Carbidopa + benserazide (work outside brain) : inhibit peripheral breakdown of L-DOPA by dopamine DECARBOXYLASE. This means that less L-DOPA is needed to be delivered as less is wasted. As less is in the system, there is a lessened chance of side effects!
  • Domperidone (works inside brain) – D2 receptor antagonist. The Chemoreceptor Trigger Zone (CTZ) is in the brainstem and dopamine acts on it to make you feel sick. Domperidone blocks this D2 activation of CTZ and therefore stops you from being sick.

Huntington's Disease

  • Hyperkinetic jerky movements initially
  • akinesia (lack of movement)  later on

Sudden brief involuntary twitches all over the body

CN & Putamen

–CN (in blue) & Putamen (pink) atrophied

-Space filled by enlarged lateral ventricles (LV in orange)

Genetics:

  • Mutations in the HD gene on the p arm of chromosome 4 (4p16.2) introduce more repeating sequences of ‘CAG’ glutamate codons (e..g CAGCAGCAGCAG etc) 
  • The excessive glutamate repeats (>40) cause the huntingtin protein to missfold and become sticky
  • mutate huntingtin protein aggregates in the CN & putamen & causes them to atrophy
  • Dominant inheritance & the disease shows genetic anticipation

Movement Pathways:

Remember, in both pathways, more dopamine = more movement.

The different stages of symptoms can be explained by different mechanisms:

  1. Initial chorea: jerky movements. (2 possible explanations)
    • CAG repeats cause too much dopamine to be produced, leading to too much movement
    • The indirect pathway degenerates first. The indirect pathway inhibits movement. Therefore by it degenerating, we get hyperkinetic movements
  2. Disease progresses to akinesia:
    • Later on, the direct pathway degenerates. 
    • As both the direct & indirect are degenerated this leads to LACK OF MOVEMENT

Treatment

The hyperkinetic movements are thought to be due to excess dopamine release.

∴ DOPAMINE DEPLETION THERAPY

e.g. Tetrabenazine (dopamine antagonist – blocks dopamine from being packaged into vesicles by blocking the VMAT transporter)

Ballism

Symptoms

🦵 Large amplitude involuntary limb movements, especially lower lib (can affect just one leg – hemiballism)

Nuclei affected

Subthalamic nucleus

Pathophysiology 

Subthalamic nucleus excites the yellow box.

IE the subthalamic nucleus makes the leash on the thalamus tighter, ie makes the thalamus more inhibited, therefore REDUCES MOVEMENT.

Destruction of the subthalamic nucleus can lead to excessive movement (hyerkinetic) aka ballism.

Treatment

N/A

Nuclei

Function

Pathologies

Striatum

(i.e. caudate nucleus + putamen)

Caudate nucleus + putamen = striatum

The striatum projects onto the Globus Pallidus via the direct and indirect pathways to control movement (see above)

 

The striatum also has D1 excitatory & D2 inhibitory receptors which respond to dopamine for the direct and indirect pathways. Overall, dopamine leads to more movement.

 

💊 The striatum has a nucleus in it called the nucleus accumbens which responds to cocaine and causes addiction! (don’t take coke all the time)

🩸Striatum is supplied by striate arteries (branch of MCA which comes from internal carortid) which also supplies the internal capsule.  Ischaemia (blockage) in striate arteries = LACUNAR STROKE. Usually causes complete contralateral hemiparalysis (e.g. in this example, paralysis of the LEFT side of the body)

😟 Huntigton’s disease: hyperkinetic, jerky movements

-initially degeneration of indirect pathway (

Internal Capsule

Not part of the basal ganglia but can be seen in the same cross sections. 

A passage for fibres to pass through. The anterior bend (‘limb’) of the internal capusle contains the fibres for worrying about stuff.

The posterior limb contains fibres for movement of the contralateral side of the body

Posterior limb:

🩸Supplied by striate arteries that come from middle cerebral artery (which in turn come from internal carotid).

ALL descending contralateral motor neurons are found here.
 These striate arteries also supply corpus-striatum, caudate nucleus & striatum

Stroke here (lacunar stroke) can lead to paralysis of the whole body!

Thalamus

Senses are processed here and sent off to other parts of the brain via reciprocal connections.

🤕 Damage to the thalamus (e.g. after a PCA stroke) can either stop you feeling pain contralaterally or cause SEVERE PAIN (severe pain = thalamic syndrome)

⚠️Absence Epilsepy Seizures (loss of awareness for a few seconds) involve thalamo-cortical circuits

Nuclei

Location

Function

Connections & Neurotransmitters

Lateral geniculate nucleus (LGN)

On the posterior of thalamus on the outside.

Visual processing.

 

Reciprocal connections to CALCARINE fissure (contralateral visual field info)

    • Visual pathway comes from retina
    • Crosses over at the optic chiasm (above the pituitary gland ) to the contralateral LGN
    • This part of thalamus has reciprocal connectionswith area 17 (V1)
    • Right geniculate nucleus connects with right side of primary visual cortex
    • Primary visual cortex – calcarine sulcus

 

Medial geniculate nucleus

On the posterior of thalamus on the inside

Auditory processing

  • Inner ear – cochlear part of VIII (8th) nerve goes to cochlear nuclei  in brainstem & synapses in inferior colliculus in midbrain 
  • medial geniculate nucleus in thalamus –> primary auditory cortex in cerebrum (buried in lateral fissure on superior surface of temporal lobe)
  • There is a tonotopic map – each part of the  cortex responds to different frequency

Ventral posterior VP nucleus

Nucleus at the very posterior of the thalamus on the lateral side (outside bit)

Somatosensory nucleus of the thalamus – sensory processing.

Maintains a somatotopic map (remembers where the sensation originated from 😮)

VENTRAL POSTERIOMEDIAL – trigeminal nerve, face & tongue organisation

VENTRAL POSTERIOLATERAL – whole rest of body –> major input to M1 motor cortex

 

INPUTS:

  • Medial lemniscus (point discrimination, vibration sense, conscious) proprioception) 
  • Spinothalamic tract (pain, temp, light, touch)
 
OUTPUTS:
  • Info goes to somatosensory areas (S1 in parietal lobe) in the brain
  • Ventral posteriolateral is a major input to the M1 motor cortex

Damage to the thalamus (e.g. after a PCA stroke) can either stop you feeling pain contralaterally or cause SEVERE PAIN (severe pain = thalamic syndrome)

Ventral lateral nucleus

Closer to the front of the thalamus, on the outside (lateral)

Motor processing

 

  • INPUT: Purkinje cell of pontocerebellum (lateral cerebellar hemispheres)
  • OUTPUT: Ventral posteriolateral is the  major input to the M1 motor cortex

Ventral anterior nucleus

At the very front of the thalamus

Motor processing

 

INPUT:

  • Receives info globus pallidus (basal ganglia)
  • & Dentate nucleus (cerebellum)

OUTPUT:

  • Basal ganglia –> Supplementary motor area  (area 6)

Dorsomedial nucleus of thalamus

Medial bit of thalamus

Emotion

  • Receive info from amygdala (emotion)
  • Output fibres go through the anterior limb of the internal capsule, to the prefrontal cortex (front bit of the brain, controls emotions)

 

Interlaminar nuclei

Nucleus inside the thalamus, underneath the internal medullary laminar

Receive information about nociception from reticular formation & keep you awake

  • Receive info from reticular formations
  • Activates striatum (basal ganglia) + neocortex to keep you awake
  • Damage to the reticular formation in the brainstem (e.g. locus cereleus) can damage this system and put you into a coma. Deep brain stimulation of these areas may help to wake you up again 🙂

Hypothalamus & Limbic System

The limbic system is made of the hippocampus, parahippocambpal gyrus, hypothalamus, amygdala & fornix. It is responsible for emotion, behaviour and memory

Mammillary Bodies

Two bulbs at the end of the fornix. Gateway to the hypothalamus

Info flows to/from hippocampus into & out of the mamillary bodies via the fornix.

The fornix is a tract of white matter that carries info between these two.

Mamillary bodies are also important in memory.

🍷🍷 In alcoholics, malabsorption of B1  –> mammillary bodies  shrivels ,  can lead to amnesia and confabulation (making up memories to fill the gaps) – AKA WERNICKE- KORSAKOFF SYNDROME

Hippocampus

Two bulbs at the end of the fornix. Gateway to the hypothalamus

Memory formation.

  • Damage to medial temporal lobe can lead to loss of episodic memory (patient HM)

Contains regions CA1, CA2, CA3,  & the dentate gyrus

Contain special neurones for spatial stuff:

  • place cells – where something is
  • Grid cells – which direction something is moving

Info can enter hippocampus through:

  1. Perforant pathway
  2. Septohippocampal cholinergic neurones

Info out of hippocampus leaves via the fornix, goes to the mamillary bodies –> anterior nucleus of thalamus

Alzheimer’s disease: misfolded evil Tau proteins can spread from entorhinal cortex, through the hippocampus, then through the temporal lobe and then the neocortex

⚠️ If Hippocampus is involved in focal seizures, you get Deja-vu

Hypothalamus

Sits below (hypo) the thymus.

Important for homeostasis.

Divided into three zones:

  1. supraoptic region,
  2. tubular region,
  3. mamillary region (the numbers are only for this diagram)

Because the hypothalamus is so close to the pituitary gland, it is able to control the release of hormones. For example, it produces GnRH – which causes the release of LH/FSH.

Nuclei/ Regions

Contains

Function

1
Supraoptic Region

Contains:

-Paraventricular Nuclei PVN

-Supraoptic Nuclei

PRODUCE ADH/OXYTOCIN  THAT GOES TO POSTERIOR PIUTATARY GLAND AND THEN TO CIRCULATION

PVN:

Important for autonomic regulation. (ESR link)

  • Synthesises ADH & Oxytocin (made by magnocellular neurones)
  • The ADH is packaged into granules with neurophysin
  • Enters the bloodstream (inferior hypophyseal circulation) via the supraoptic hypothalamic tract
  • ADH makes your wee more concentrated (more ADH when you are thirsty)
  • 🐣🐣🐣 When giving birth, contractions activate stretch receptors
  • This has positive feedback on the neurosecretary cells in the hypothalamus
  • More OXYTOCIN IS RELEASED
    • Targets the myometrium making the contractions even more forceful = 👶

2
Tubular Region

//////// Makes up the tubular-infiundibulary region

Just above the stalk of the pituitary gland (infundibular stalk)

Contains:

-Arcuate Nucleus

-Tubular Mamillary Nucleus (because it is next to the mamillary bodies of the fornix)

HUNGRY/SLEEPY CONTROL ZONE

ARCUATE NUCLEUS:

  • Controls Appetite by having leptin receptors (adipocytes release leptin to make you feel full/satiated)
    • Fibres cross at midline here
  • Also produces dopamine which acts to inhibit the release of prolactin (lactating hormone 🍼) AKA DOMINANT NEGATIVE CONTROL
    • ie Prolactin is basically always switched off (by dopamine) unless you are pregnant
    • Therefore anti-psychotics that block D2 dopamine receptors (e.g. Risperidone, apomorphine) also stop arcuate nucleus from producing dopamine = lead to the side effect of high prolactin 
    • =hyperprolactinaemia! (can cause unwanted lactation)

 

TUBULAR MAMMILARY NUCLEUS:

  • Tubular mamillary nucleus controls wakefullness.
  • The only histamine nucleus in CNS. 
  • Therefore antihistamines can make you sleepy
  • Area damaged in ENCEPHALITIS LETHARGICA – sleeping for upto 20hrs a day!
  • The interlaminar nuclei of the thalamus also control sleepiness

3
Posterior/ Mammillary Region

Contains Mamillary Nuclei

TEMPERATURE ZONE

  • Mamillary nuclei = memory & thermoregulation
    • Lesions here can cause HYPOthermia (hypothalamus –> hypothermia). 

Cerebellum

The cerebellum is the mini-motor brain that sits at the very back of the brain, posterior to the brainstem.

It is responsible for fine tuning of motor movements, and receives  inputs such as proprioception & error signals, and outputs via the DCN to different motor areas. 

Cerebellar lesions/strokes lead to DANISH:

  • Dysdiadochokinesia (inability to rapidly pronate/supinate hand)
  • Ataxia (gait and posture)
  • Nystagmus (eye muscle movements)
  • Intention tremor
  • Speech problems
  • Hypotonia (decreased muscle tone)

 

Mossy Fibres

  • Carry Error Signals to the cerebellum 
  • SOURCES:
    • Pons –> Middle Cerebellar Peduncle (e.g. vestibular 👂)
    • Dorsospinal Cerebellar Tract –> Inferior Cerebellar Peduncle (proprioception 👋 )
  • ROUTE:
    • Fibres arise from either middle/inferior cerebellar peduncle then:
    • Go into granule layer of the cerebellar cortex
    • Connect to granule cell
    • Granule Cell projects the mossy fibres upwards into the molecular layer of cerebellar cortex
    • From here, the mossy fibres become lots of fibres running parallel to each other (parallel fibres)
    • Connect with purkinje cells to output
  • PURKINJE CELL OUTPUT
    • LOTS of parallel fibres connect to ONE purkinje cell
    • Purkinje cell has one output fibre to the deep cerebellar nuclei to make adjustments

Climbing Fibres

  • Carry Error Signals to the cerebellum e.g. retinal slip  👀
  • SOURCES:
    • ALL ARISE FROM THE INFERIOR OLIVE 🫒
    • Olive trees climb!
 
  • ROUTE:
    • Fibres come from the inferior olivary nuclei in the olives in the medulla
    • Cross the midline (CONTRALATERAL) and go to inferior cerebellar peduncle
    • From here, they form climbing fibres
    • These climb directly to the purkinje cell (without splitting into parallel fibres)
 
 
  • PURKINJE CELL OUTPUT
    • ONE CLIMBING FIBRE TO ONE PURKINJE CELL (1:1)
    • Purkinje cell has one output fibre to the deep cerebellar nuclei to make adjustments

Nuclei/ Cerebellum landmark

Location

Function

Connections & Neurotransmitters

Anterior Lobe

The top bit of the cerebellum

Parts I-V (1-5) of cerebellum

Problems here lead to GAIT ATAXIA

 

    • The anterior lobe of the cerebellum can be damaged in alcoholics (in Korsakoff’s syndrome)
    • Alcohol = malabsoprtion of Vit B1 = brain damage e.g. anterior lobe of cerebellum

Vermis

Thing that runs along the middle of the cerebellum (separates left/right hemispheres)

Spinocerebellum

Receives info about non-conscious proprioception (that you don’t consciously think about)

  • Receive a lot of information from spinocerebellar tracts (e.g. conscious proprioception, discriminative touch, temperature, pain etc) .

Anterior lobe vermis particularly sensitive to alcohol misuse. Lesions here can cause ataxia of gait

INPUT: Spinocerebellar tracts

  • These tracts contain proprioceptive info
  • Info comes from proprioceptive neurones, which go to the dorsal column, synapse at Clarke’s column in the grey matter (Cell bodies) 
  • This neuron then goes to the white matter (tracts) and travels up the dorsal spinocerebellar tract
  • The tract goes to the inferior cerebellar peduncle –> vermis
  • Fibres becomes mossy fibres, then parallel fibres 
  • Project onto one purkinje cell –> Globose/Emboliform nuclei

OUTPUT:

  • Controls dorsolateral descending systems (rubrospinal and corticospinal)

Lateral Lobes of cerebellum

Left/Right side of the cerebellum

Make up the pontocerebellum (fine movement)

OUTPUT:

  • Outputs information about planning movements to the  Dentate Nucleus
  • Dentate nucleus has efferent projections (outputs) which leave via the SUPERIOR CEREBELLAR PEDUNCLE
  • These go to the ventrolateral nucleus of thalamus & crosses the midline
  • The ventrolateral nucleus of the thalamus projects to the motor (M1) and premotor (area 6) cortex in the cerebrum
  • The cerebrum sends these motor signals out via corticospinal tracts which cross at the pyramids
  • Because there is double crossing, the cerebellum has ipsilateral motor control

Floccular-nodular Lobe of Cerebellum

Part X of cerebellum – at the inferior surface 

Makes up the vestibulocerebellum (along with a small part of the vermis)

Receives input from the vestibular labyrinth (three loops in the ear filled with endolymph and the utricle and saccule) , and projects directly to vestibular nuclei .

-Controls balance & Eye movements

 

Damage = deficits in visual tracking , nystagmus (oscillation of eye movements), vestibulo ocular reflex errors and balance problems

The vestibulocerbellum receives error signals from the eyes and ears:

 

floccular-nodular lobe

-👂 semi-circular canals in ears filled with endolymph. Balance error signals carried by CN VIII into mossy/parallel fibres: 

Small part of vermis

-👀 error signals about retinal slip (eye movement) via pretectal nucleus –> inferior olive —> Climbing fibres 

-Vermis also receives input from neck and trunk

From here, the error signals (mossy/climbing fibres) project onto Purkinje fibres which then output the error information to the FASTIGIAL NUCLEUS

After going to the fastigial nucleus, the purkinje axons then leave the cerebellum:

floccular-nodular lobe

Project directly to

  • vestibular nuclei in the dorsolateral medulla (supplied by PICA)

  • Reticular formation

Small part of vermis

Output through reticulospinal, vestibulospinal and corticospinal fibres through the inferior cerebellar peduncle

Superior cerebellar peduncle

The most superior peduncle of the cerebellum, near choroid plexus of 4th ventricle

The cerebellar peduncles are masses of tissue that connect the brainstem (pons) to the cerebellum

OUTPUT (efferents):

 -lateral hemispheres of the cerebellum (pontocerebellum) control fine movement

-These fibres exit the cerebellum and cross at the superior cerebellar peduncle (contralateral)

  • Gives small input to red nucleus (midbrain)
  • Gives larger input to thalamus and onto motor cortex (ventrolateral thalamus –> M1 – precentral gyrus & ventroanterior thalamus –> area 6 premotor cortex PMC)
  • Also project to reticular formation in brainstem

Middle Cerebellar Peduncle

At the level of the pons.

The biggest of the three cerebellar  peduncles.

The cerebellar peduncles are masses of tissue that connect the brainstem (pons) to the cerebellum

SOURCE OF MOST MOSSY FIBRES

The biggest cerebellar peduncle that connects the pons to the medulla

Because it is the biggest peduncle, it is the source of most of the mossy fibres.

The middle cerebellar peduncle is very visible (in purple) when you do a cross section of the pons:


Inferior Cerebellar Peduncle

Lowest cerebellar peduncle at the level of the lower pons/very top bit of the open medulla.

The cerebellar peduncles are masses of tissue that connect the brainstem (pons) to the cerebellum

SOURCE OF MOSSY FIBRES FROM DORSOSPINAL CEREBELLAR TRACT 

Dorsospinal cerebellar tracts contain proprioceptive information

They travel up from C8-L2 all the way to the inferior cerebellar peduncle, which connects them to the spinocerebellum (intermediate zone around vermis).

From here they turn into mossy fibres and then go to purkinje cells (apart from the dorsospinal cerebellar tracts, most mossy fibres comes from the middle cerebellar peduncle)

Cerebellar Cortex:

Granule Layer

The outer bit of the cerebellum is folded into folia which contain the grey matter. This is the cortex which is divided into three sections. The granule layer is the bottom most section of the cerebellar cortex.

Contains granule cells.

Mossy fibres project onto here. 

The granule cells then go upwards to the molecular layer where they split into parallel fibres

INPUTS: 

Mossy fibres from pons/dorsospinal cerebellar tract

 

OUTPUTS:

Mossy fibres synapse onto granule cells which then project upwards into the molecular layer and become thousands of parallel fibres.

 

LOADS of parallel fibres then go into one purkinje output cell

Purkinje Layer

The purkinje layer is the middle section of the cerebellar cortex.

Contains purkinje cells. These are the main output cells of the cerebellum.

INPUTS:

  • Direct input from climbing fibres (arise from the inferior olivary nuclei). 1 climbing fibre : 1 cell
  • Mossy fibres split into thousands of parallel fibres. LOADS of parallel fibres connect to ONE purkinje cell

 

OUTPUTS:

Purkinje cells have efferent fibres to the deep cerebellar nuclei (DCN)

Molecular Layer

 The molecular layer is the top/outermost section of the cerebellar cortex.

Contains parallel fibres

At the molecular layer, mossy fibres split into thousands of parallel fibres and then loads of these parallel fibres connect to just one purkinje cell.

The purkinje cell then goes onto the DCN.

Deep Cerebellar Nuclei: Don't Eat Greasy Food

Dentate | emboliform | Globose | Fastigial

Dentate Nucleus

Outer most nuclei of the DCN (in green)

 

Main output nuclei of lateral cerebellum (pontocerebellum)

–> Ipsilateral control of movement (via thalamus)


Input from ventral lateral/ventral anterior nucleus of thalamus

Fastigial Nuclei

gfgf

Control balance 

Receives info from floccular-nodular lobe and sends axons to

  • vestibular nuclei  (dorsolateral medulla) via vestibulospinal tract &
  • reticular formation

Brainstem

The brainstem is the bit of the brain that connects to the spinal cord – it is responsible for a lot of the non-conscious stuff that keeps us alive.

It is made of three sections:

  • Midbrain (aka mesencephalon): cerebral peduncles containing CST (shown in green), substantia nigra, red nucleus, DCMLT, STT, midbrain reticular formation, periaqueductal grey, superior/inferior colliculi

 

  • Pons can be divided into layers based on the connections to the cerebellum (mini motor brain) called the cerebellar peduncles
      • Superior cerebellar peduncles
      • Middle cerebellar peduncles (these are the biggest)
      • Inferior cerebellar peduncles – most inferior bit of the pons

 

  • Medulla the most inferior (caudal – closer to the spinal caud!) bit of the brainstem. Has distinct curly bits which are the olivary nuclei
      • SUPERIOR: OPEN MEDULLA 💧💧💧 The upper bit of the medulla has the 4th ventricle (last collection of CSF in the brain) and is called the open medulla.
      • INFERIOR: CLOSED MEDULLA ⛔💧⛔  The 4th ventricle narrows in the  lower bit of the medulla to become the central canal of the spinal cord. Therefore there is no more 4th ventricle/fluid stuff in the inferior bit of the medulla

After the medulla is the spinal cord

The cross sections in the diagram above have been orientated as if you are standing behind someones brainstem and looking at them (posterior view). 

Normally neuroanatomy  diagrams shows cross-sections the other way but that is harder to visualise – so dont be confused!

Nuclei

Location

Function

Connections & Neurotransmitters

Pathologies

Midbrain nuclei

  • Red nucleus
  • Superior colliculi
  • Oculomotor 

The oculomotor CNIII nucleus contains a parasympathetic bit called the Edinger-Westphal nucleus

Pupillary Light Reflex (high yield)

–> Shine a light into one of someone’s eyes,  BOTH their pupils will constrict:

      1. Ganglion cells in the retina detect light
      2. Info carried by optic nerve
      3. Pretectal nucleus goes to both edinger-westphal nuclei
      4. Info goes to Edingher-westphal nucleus on contralateral side 
      5. Short Ciliary nerves = sympathetic  ganglion –> oculomotor
      6. Sphincter pupillae muscle causes pupil to constrict. This is innervated by CNIII

If you have a CNIII third nerve palsy (down and out), the sphincter pupillae muscle won’t be able to contract, so therefore the pupil will be fixed and dilated 🙁 

Locus cereleus

Just in front of superior cerebellar peduncle, near the 4th ventricle

Have an analgesic effect on:

  • pain 🤕
  • wakefulness 😴
  • memory 🧠

NA (noradrenergic connections) all over the brain

Locus coereleus releases NA which acts on a2-adrenoreceptor.

This is part of inhibitory pain controls 🙂 

Inhibitory pain controls of locus coereleus lost in chronic pains

In contrast to the locus coereleus, the rostral ventral medial medulla (RVM medulla) WORSENS PAIN BY RELEASING 5HT 🙁

Trigeminal sensory nuclei

The three sensory branches of the trigeminal nerve (V) comes into the brainstem via the trigeminal ganglion.

  • The ganglion then splits up into three separate nuclei

– mesencephalic nucleus in rostral end (top bit – rostral is near the NOSTRIL) in midbrain,

 

-Chief nucleus in middle (upper pons)

= discriminative touch of face

-Spinal nucleus at the caudal end of the brainstem (continous with the dorsal horn of  spinal cord – hence called SPINAL!). The spinal nucleus is (dorsal, lateral) at the level of the lower pons/ upper open medulla

Chief nucleus of trigeminal nerve = discriminative touch info about the face via AB fibres

Spinal nucleus controls nociceptive (pain sensing) bits of trigeminal nerve via C fibres

  • ⚡ Anterior 2/3 of tongue supplies somatosensory information via lingual nerve (mandibular branch) to spinal nucleus
  • 🦠 Shingles ==> post herpetic neuralgia (i.e. nerve pain after you get herpes)  -often spreads unilaterally on one side of the route of a section of trigeminal nerve

 

  • 🩸 The superior cerebellar artery can irritate the trigeminal nerve and cause trigeminal neuralgia – extreme pain in face 

 

 

SPINAL NUCLEUS STROKES

  • 🩸 Spinal nucleus supplied by AICA/PICA
  • ⚠️ AICA/ PICA STROKE/LESIONS WILL DAMAGE SPINAL NUCLEUS ==> CAUSE LOSS TO TRIGEMINAL FUNCTIONS
  • ⚠️ Ipsilateral face anaesthesia (numbness when chewing)

Nuclei

Location

Function

Connections & Neurotransmitters

Pathologies

Medial Leminiscus

Found throughout brainstem.

Open medulla:

Receives sensory info about vibration, proprioception & discriminative touch from contralateral side of the body

( fibres ipsilateral at spine but cross at medulla aka hindbrain)

 

 

⚡ At the level of the open medulla, it contains internal arcuate fibres.

These fibres go to ventral posterior nucleus of thalamus (which is quite close to the brainstem). From here info gets relayed to somatosensory areas of cerebral cortex (e.g. post-central sulcus) via RECICIPIRICAL CONNECTIONS

 

The post central sulcus in the cerebrum helps work out what objects are via discriminative touch : STEROGNOSIS

• TABES DORSALIS – most common form of neurosyphilis – stamping gait due to lack of proprioception in dorsal column

• FRIEDREICH’S ATAXIA: genetic degenerative of DC tracts & spinocerebllar

• BROWN-SEQUARD SYNDROME – hemisection of spinal cord often due to stabbing – loss of ipsilateral touch and proprioception sensation on side of inury due to cutting of DCML

Complete loss of both nociceptive (spinothalamic) & proprioceptive (DCML) sensation at the level of the injury.

Raphe Nuclei Part of reticular activating system

There are several nuclei that make up the Raphe nuclei that are found throughout the brainstem. 

Raphe Magnus is found somewhere at the lower pons/upper bit of the medulla (open medulla) – i.e. where there is the 4th ventricle, and olivary nuclei.

 

Modulate pain

 

Also modulates  the mesencephalic locomotor region (MLR) – which controls walking speed. 🚶‍♂️–>🏃‍♂️

Use 5HT (serotonin) as a neurotransmitter.

 

 

Medial Longitudinal Fasiculus

 Open Medulla

Integrates all the eye nerves together (CNIII, CNIV, CNVI) & connects them to CNVIII (8) – for vestibulo-ocular reflex.

Receive info DIRECTLY from the fastigial nucleus (DCN) from the floccular-nodular lobe in cerebellum – originally from CNVIII (8)

PICA Stroke – balance problems/nystagmus

Vestibular nuclei

Dorsolateral medulla.

Receive information about balance

Receive info DIRECTLY from the fastigial nucleus (DCN) from the floccular-nodular lobe in cerebellum – originally from CNVIII (8)

PICA Stroke – balance problems/nystagmus

🍩 Nucleus of the Solitary Tract NTS 🍩

Dorsolateral open medulla (superior bit of the medulla).

Baroreceptor & taste

Input:

  • 🫀 Baroreceptors in aortic arch/ carotid sins
  • NTS decreases BP by increasing parasympathetic drive & leading to the rostral ventral lateral medulla RVLM to be inhibited (decreasing sympathetic drive)

Also has endings of visceral afferent fibres of taste & gut – THINK! WHEN 

🫒 Olive

Anterior swelling of the medulla

Inferior Olivary Nuclei: Source of all climbing fibres which contain error signals and go to the cerebellum, projecting directly onto the purkinje cells

Superior Olivary Nuclei: auditory processing & integration

Climbing Fibres

  • Carry Error Signals to the cerebellum e.g. retinal slip  👀
  • SOURCES:
    • ALL ARISE FROM THE INFERIOR OLIVE 🫒
    • Olive trees climb!
 
  • ROUTE:
    • Fibres come from the inferior olivary nuclei in the olives in the medulla
    • Cross the midline (CONTRALATERAL) and go to inferior cerebellar peduncle
    • From here, they form climbing fibres
    • These climb directly to the purkinje cell (without splitting into parallel fibres)
 
 
  • PURKINJE CELL OUTPUT
    • ONE CLIMBING FIBRE TO ONE PURKINJE CELL (1:1)
    • Purkinje cell has one output fibre to the deep cerebellar nuclei to make adjustments

Fibres, Nerves & Tracts

Auditory processing: cochlear nuclei, MGN, superior & inferior colliculus , superior olivary nuclei.

 

 

Auditory Summary Video (9 mins)

Auditory Processing in Depth (50 mins):

Eye Muscle Movements:

Visual Field Pathways Video:

Interactive Version of Visual Processing:

Tracts

Tract

Pathway

Function

Crossed over?

Pathologies

Corticospinal Tract (CST)

Pathway

Motor Tracts

Lateral corticospinal: fine motor control – wiggling fingers

Ventral Corticospinal: postural muscle

Lateral Corticospinal Tracts cross over at the pyramids of the medulla

If (lateral) corticospinal tracts are damaged after they have crossed at the pyramids of the medulla, then symptoms will be IPSILATERAL (i.e. if damaged in the spine) . If damaged before they cross (in the brain/UMN), symptoms are contralateral

Strokes:

-PCA (contralateral hemiplegia – mostly in face)

–Brown-Sequard Syndrome🔪🔪

Hemisection of spinal cord often due to stabbing

at the level of & below the lesion: IPSILATERAL fine motor los

Ventral (anterior) Spinal Artery Stroke

–Syringomyelia rarely affects the CST – if the syrinx grows outwards to the lateral CST.

UMN ALWAYS INVOLVE CORTICOSPINAL TRACTS. LOSS OF CST IN UMN LESIONS CAUSES HYPERREFLEXIA

Spinothalamic Tract (STT)

Pathway

Pain/temperature info enters via the dorsal column, goes through the grey matter and crosses-over near the spinal canal, and then goes upto S1.

Therefore carries contralateral pain/nociception/temperature info

Pain / Temperature Sensory Tracts

Lateral STT: contralateral pain ( nociception) & temperature 

Anterior STT: contralateral crude touch – can be tested with a cotton wool.

STT can be removed in a procedure called ventrolateral cordotomy to stop terminally ill pateitns from feeling pain 

Both anterior/lateral STT cross at grey matter in spinal cord

LOSS OF PAIN OR PRESSURE  SENSATION

 

Strokes:

ACA (contralateral loss in leg 🦵),

MCA (contralateral loss in face 😮/ arms 💪),

AICA (contrateral loss in  body/Ipsilateral loss in face😮),

Bilateral loss in Anterior Spinal Artery stroke

Brown-Sequard – contralateral loss below lesion, bilateral at level of lesion

Syringomyelia – bilateral as both sides are blocked from crossing over by the syrinx

Dorsal Column Medial Lemniscus Tract

Pathway

Fibres go to the VP nucleus of the thalamus –> S1 somatosensory areas via reciprocal connections.

Vibration & Proprioception

-test vibration using a 128Hz tuning fork 🍴 in sensory exam

-test proprioception by pushing big toe either up or down and asking patient to tell you which way its moving.

Crossed at the medulla in brainstem

• TABES DORSALIS – most common form of neurosyphilis – stamping gait due to lack of proprioception in dorsal column

• FRIEDREICH’S ATAXIA: genetic degenerative of DC tracts & spinocerebellar tracts

•STROKES:

ACA (contralateral leg🦵),

MCA (contralateral face 😮/ arm 💪),

Brown-Sequard Syndrome – bilateral at level of lesion, ipsilateral below the lesion

 

Not affected in VSA stroke / syringomyelia 🙂

Trigeminal Touch Pathway

Pathway

Trigeminal nerve (V). Projects to PRINCIPAL/CHIEF SENSORY NUCLEUS

  • Then crosses at midline, joins medial leminsical pathway
  • Then projects to Ventral posterior (VP) nucleus in thalamus  just like DCMLP (but more medially in the nucleus)
  • Then projects onto S1

Same as dorsal column but for the face

Crosses at midline from cheif sensry nucleus 

Pain fibres

C

Smallest

Pain, itch, temperature

Ad

Larger

Fast pain, temperature

AB

Even larger

Skin mechanoreceptors, touch

Aa

Largest

Proprioceptors

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