Neuroscience And Mental Health Flashcards
State where the CNS and PNS arise from. State the main cells in each differentiation.
The wall of the neural tube lined with the neuroepithelium forms the CNS. Folding of neural plate forms the neural tube. Neural tube closing up forms the walls of the neural canal. The neuroepithelium of the canal forms CNS.
Differentiation of neuroepithelium
Neuroblasts = all neurones with cell bodies in CNS
Glioblasts = astrocytes (neurotransmission, support, form BBB), oligodendrocytes (myelin sheath, more rapid a.p. by saltatory conduction)
Ependymal cells = lining ventricles and central canal of spinal cord
Neural crest forms the PNS.
Differentiation of neural crest cells
Sensory neurones of dorsal route ganglia (lie next to spinal cord all the way down back)
Postganglionic autonomic neurones
Schwann cells
Non-neuronal derivatives .e.g. melanocytes
Explain the proliferation and differentiation of the neuroepithelium.
Massive proliferation of cells of the wall of neural tube. Cells actively dividing from inside to outside.
Differentiation: from inside to outside: ependymal layer (developmental cells lie here, migrate to grey matter laminarly) -> grey matter -> white matter (contains neuroblasts -> myelinated axons and processes)
When looking at surface of brain, you see grey matter (nerve cell bodies), white matter seen when dissected, ependymal = ventricles
Layers of neural tube from ventral to dorsal:
Floor plate, white matter (marginal layer), grey matter (mantle layer), ependymal layer (germinal layer), neural crest, roof plate
Spinal cord: white outside, grey core
Brain: grey outside, white inside
Differentiation controlled by:
Signalling molecules, secreted by surrounding tissues, interact with receptors on neuroblasts
Control migration and atonal growth by attraction and repulsion (tropic and inhibitory factor balance)
Depends on conc gradient and timing
Explain the development of the spinal cord.
Diagram
Explain the development of the brainstem.
Diagram
Explain the development of the brain.
Diagram
Developing cortex
Describe the developmental disorders.
Normal development depends on the coordinated completion of several complex processes e.g. proliferation, differentiation, migration, axon growth and synapse formation)
Genetic mutation and environmental factors such as mother’s lifestyle, diet and teratogens (agents known to interfere with normal developmental process) can interfere with these processes
Neural tube defects: folic acid prior to pregnancy prevent this.
Top defects
Craniorachischisis - completely open brain and spinal cord
Anencephaly - open brain and lack of skull vault, anterior part of neural tube has not fused properly and brain has not developed - not compatible with life
Encephalocele - herniation of meninges outside cranial cavity
Base defects
Spina bifida occulta- closed asymptomatic NTD in which some of the vertebrae are not completely closed.
Closed spinal dysraphism - deficiency of at least two vertebral arches, here covered with a lipoma, herniation covered by fat
Neural stem cell defects
In hippocampus, found in adults
Some neural cells die by apoptosis, degenerative diseases - atrophy
Describe the spinal cord segments.
31 spinal segments and 31 pairs of spinal nerves 8 cervical 12 thoracic 5 lumbar 5 sacral 1 coccygeal
Nerves leave the vertebral column through intervertebral foramina (holes between vertebrae), pair on either side, pair of nerves leave
Enlargements for innervation of the limbs
Cervical (C3-T1) -upper limb
Lumbar (L1-S3) -lower limb
Discrepancy between spinal levels and vertebral levels
Cervical nerves above vertebra until C8, there are 7 cervical vertebrae and 8 cervical nerves, C8 below C7 so afterwards below vertebrae.
As you go down SC, nerves become more distanced from their vertebrae.
Spinal injury at T8 = T8 segment of spinal cord is working well
SC has same no. Of segments as vertebral column but is shorter, coccygeal part is level with lumbar region.
Describe the meninges and relation to epidural/spinal anaesthetic.
From outside to inside dura -> arachnoid -> pia
No space between dura and skull in cranial cavity but there is space between dura and vertebral column so anaesthetics are injected into epidural space of spine.
Subarachnoid space in brain filled with CSF in ventricles entering in and out of sulci. CSF produced in ventricles through foramina in 4th ventricle and enter subarachnoid and into spinal cord/canal.
In spinal cord, can pace anaesthetics and remove CSF as part of lumbar puncture.
Safer and clinically relevant:
1) access to spaced which exists in vertebral column but not skull
2) spinal cord doesn’t extend as far down as vertebral column and ends at around L2, below that epidural space is not filled with spinal cord that may be damaged by needle. Nerves just floating around in subarachnoid space so can move out of the way.
Pia ends at end of SC and small filament called filum terminale (extension of pia) that anchors SC to sacrum.
Can assess CSF infection e.g. meningitis
Can introduce compounds such as spinal blocks and anaesthetics
State what a myotome and dermatone is.
Dermatome: an area of skin innervation by one single spinal nerve or spinal segment. (Single pair)
Myotome: muscles innervated by one single spinal nerve or spinal segment.
Describe a cross section of the spinal cord.
Rootlets make up roots
Anterior root and posterior root join to form spinal nerve (mixed sensory and motor) which then divides into posterior and anterior rami.
Gray matter: cell bodies
White matter: tracts
4 parts overall: Posterior (dorsal) horn (gray) - two types of neurones: 1) those with axons that project to the brain (projection neurones) 2) those with axons that remain in the spinal cord (interneorunes) Anterior (ventral) horn (gray) Posterior column (white) Anterior column (white)
Posterior median sulcus divides posterior surface of spinal cord into two halves
Anterior median sulcus divides anterior surface of spinal cord into two halves.
Posterolateral sulcus - entry point of the posterior root (sensory)
Anterolateral sulcus - exit point of the anterior root (motor)
Explain the gray matter.
Discriminative touch and proprioception
Sensory fibres will enter the dorsal horn and travel in dorsal columns without synapsing in posterior horn.
Pain and temperature
Fibres enter dorsal horn and may travel 1-2 segments up or down in the Lissauer tract (Sensory fibres carrying pain and temperature will ascend or descend several spinal cord levels before synapsing in dorsal horn) and then synapse in nucleus proprius. Fibres that cross midline of anterior commissure and travel in the spinothalamic tract.
Motor
Alpha motor neurones are located in the anterior horn, They exit the spinal cord and travel to their target muscles, Interneuron circuits in the anterior hormone filter descending motor information and are part of localised reflex circuits.
Explain the white matter.
Major tracts of spinal cord:
Fasciculus gracilis: sensory (fine touch, vibration, proprioception) from ipsilateral lower limb.
Fasciculus cue at us: sensory (“) from ipsilateral upper limb.
Spinocerebellar tract: proprioception from limbs to cerebellum
Lateral corticospinal tract: motor to ipsilateral anterior horn (mostly limb musculature) 85%
Anterior corticospinal tract: motor to ipsilateral and contralateral anterior horn (mostly axial musculature - muscles of head and trunk) 15% - don’t cross over
Spinothalamic tract: pain and temperature from contralateral side of the body. (Spin to brain from opposite side of body)
CST carry info from brain to muscles for voluntary movement.Motor cortex in gyrus which sits in front of central sulcus sends fibre down into medulla at which it crosses to other side (85% cross to limbs, 15% stay on same side to trunk muscles)
Anterior white commissure: pain and white temperature fibres cross. Anterior corticospinal tract fibres cross.
Explain the main sensory pathways.
3 different neurones between skin and brain:
1) brings info into spinal cord (primary sensory neurone)
2) spinal cord to thalamus (secondary)
3) thalamus to cortex - register sense - pain, temp, touch .etc. (Tertiary)
Secondary neurone is what primary synapses onto. When synapse occurs, secondary neurone crosses over to the their side of body; synapse occurs in spinal cord (pain/ temp)/ medulla - synapse similar to crossing of motor neurone (touch/proprioception)
Synapse of tertiary in thalamus in both pathways.
All pathways bilateral for left and right.
Dorsal column pathway - discriminative touch, vibration, proprioception (gracilis, cuneatus)
Spinothalamic tract - pain and temperature
Dorsal root ganglion is collection of cell bodies of primary running side of spinal cord.
Explain reflex pathways.
Reflex bigger: stroke
Smaller: peripheral nerve lesion
Explain autonomic outflow.
Cord - sympathetic (thoracolumbar)
Brain and sacral- parasympathetic
Generally, bacterial and posterior horns, sometimes in thoracolumbar region there is extra intermediate horn - site of the motor neurones of sympathetic nervous system.
Describe spinal lesions.
Factors affecting severity of spinal lesion:
Loss of neural tissue
Vertical level
Transverse plane
Loss of neural tissue
Usually small if due to trauma
Can be more extensive e.g. metastases, degenerative disease
Effect of spinal lesion depends on how much tissue is lost.
Vertical level
Higher the lesion e.g. fracture, greater the disability
Closer to head, more of the body effected
Repair or bypass = treatment
Transverse plane Most lesions are not complete Posterior - affecting sensory Anterior - affecting motor Contralateral - opposite side Ipsilateral - same side of innervation And tracts involved: Dorsal columns - sensation to touch Spinothalamic - sensation to pain and temp Lateral corticospinal - movement
Injury to lateral corticospinal tract
Stage 1: spinal shock: loss of reflex activity below the lesions, lasting for days or weeks = flaccid paralysis
Stage 2: return of reflexes: hyperreflexia and/ or spasticity = rigid paralysis (much more excitable neurones, returns with greater vigour - more intense + quicker)
Brown-Sequard syndrome: with unilateral lesions the relationship of the deficit to the lesion depends on where the tract decussates. (Same side or opposite depending on where in each tract)Usually pain and temp sensation loss contralateral and proprioception ipsilateral.
Explain the blood supply to the brain.
Brain has high demand for O2, CO, liver glucose and therefore vulnerable if blood supply impaired.
Two sources:
Internal carotid arteries
Vertebral arteries - at back of neck and associated with cervical vertebrae. 4 arteries come together at base of brain to form anastomotic circuit of vessels called Circle of Willis. Branch of Circle of Willis known as cerebral arteries.
Arteries to brain and meninges
- Common carotid artery splits into external and internal carotid at C3/C4. External supplies face and surface soft tissue and has lots of branches. Internal is unbranded and travels up through base of skull and emerges in anterior part of cranial cavity and supplies anterior part of circulation.
- 1st branch of subclavian arteries vertebral artery which goes through transverse foramina of cervical vertebrae -> base of skull -> pass through foramen magnum -> joins rest of blood supply.
Arteries of brain
Diagrams
Completely occluded carotid artery must be removed by endarterectomy (remove plaque) to avoid compensatory flow
Describe the venous drainage of the brain
Cerebral veins
Venous sinuses - made from folds of the dura mater. All drain to back of head and into internal jugular vein found next to carotid arteries in neck.
Dura mater
Internal jugular vein
Diagram
Explain the consequences of insufficient blood supply to the brain.
Give the causes of occlusions.
Stroke
Cerebrovascular accident (CVA)
Rapidly developing focal disturbance of brain function of presumed vascular and of > 24 hours duration.
Infarction (85%) or haemorrhage (15%)
Transient ischaemic attack (TIA)
Rapidly developing focal disturbance of brain function of presumed vascular origin that resolves completely within 24 hours.
Temporal blockade to blood vessel - atherosclerotic debris broken off or blood clot broken up quickly - can mean risk for stroke.
Infarction
Degenerative changes which occur in tissue following occlusion of an artery - area of dead tissue which has lost its blood supply.
Cerebral ischaemia
Lack of sufficient blood supply to nervous tissue resulting in permanent damage if blood flow not restored quickly.
Hypoxia/ anoxia
Causes of occlusions:
Thrombosis: formation of a blood clot (thrombus)
Embolism: plugging of small vessel by material carried from larger vessel .eg. Thrombi from the heart or atherosclerotic (build up of fatty deposit inside lining of vessels) debris from the internal carotid. (can lead to atheroma -> infarction)
Give the main risk factors of stroke and describe the different types of strokes.
Age
Hypertension - haemorrhagic aneurysm -> weakening -> burst
Cardiac disease - static blood around valves -> thrombi
Smoking
Diabetes mellitus
Problem with anterior cerebral artery (supplies motor cortex of lower limb)
Paralysis of contralateral leg > arm > face
Disturbance of intellect, executive function (decision making) and judgement (abulia- frontal lobe)
Loss of appropriate social behaviour
Middle cerebral artery
“Classic stroke”
Contralateral hemiplegia (paralysis of one side of the body): arm > leg
Contralateral hemisensory deficits - behind central sulcus is main sensory cortex
Hemianopia - blindness over half field of vision
Aphasia (L sided lesion) - impairment of language e.g. expressive aphasia - difficulty recalling words
Also supplies deep structures which may not be seen on surface so can get complete hemiparesis (weakening of one side of body)
Posterior cerebral artery
Visual deficits (largely occipital)
Homonymous hemianopia - loss of visual field on same side of both eyes because only one side of cortex affected
Visual agnosia - e.g. face recognition - prosopagnosia
Lacunar infarcts
Lacunae are small cavities found in brain, in post-mortem represent small strokes which have happened in life
Appear in deep structures as a result of small vessel occlusion
Deficit is dependent on anatomical location
Hypertension
Haemorrhagic stroke
4 types:
Extradural (between dura and skull - closest to skull) - trauma, immediate effects, middle meninges arterial bleed pushes dura away from skill, starts putting pressure on brain, raise in intracranial pressure, shut down of brain steam sensors as pushed down
Subdural - trauma (movement + bridging veins are ruptured), delayed effects - blood can accumulate without having any noticeable effects initially, history of head injury and unconsciousness kept in case
Subarachnoid - ruptured aneurysms, middle of 3 endings - all vessels at base of brain in subarachnoid space - berry aneurysm
Intracerebral - spontaneous hypertensive
Describe a syncope and what happens to the brain during hypoglycaemia.
Syncope = fainting, is a common manifestation of reduced blood supply to the brain.
Has many causes including low blood pressure, postural changes, vaso-vagal attack (sight of blood/ extreme emotional stress), sudden pain, emotional shock etc.
All result in a temporary interruption or reduction of blood flow to the brain.
Glucose is principle energy source for the brain because it cannot store, synthesise or utilise any other store of energy (although in starvation, ketones can be metabolised to a limited extent)
During hypoglycaemia, an individual appears disoriented, slurred speech, impaired motor function.
If glucose conc. falls below 2 mM it can result in unconsciousness, coma and ultimately death.
State the two ways cerebral blood flow is regulated by.
Mechanisms affecting total cerebral blood flow.
Mechanisms which relate activity to the requirement in specific brain regions by altered localised blood flow.
Explain how total cerebral blood flow is regulated.
Total cerebral blood flow is autoregulated between MABP of 60-160 mmHg.
The arteries and arteries dilate or contract to maintain blood flow.
Stretch-sensitive cerebral vascular smooth muscle contracts at high BP (limits blood flow) and relaxes at lower BP (opens up vessels - more blood flow)
Below this auto regulatory pressure range, insufficient supply leads to compromised brain function
Above this autoregulatory pressure range, increased flow can lead to swelling of brain tissue which is not accommodated by the closed cranium, therefore intracranial pressure increases - dangerous
Explain regulation of local cerebral blood flow.
Local brain activity determines the local O2 and glucose demands therefore require local autoregulation by:
Neural control
Chemical control
Arteries enter CNS tissue from branches of surface pail vessels. These branches penetrate into the brain parenchyma branching to form capillaries which drain unto venues and veins which drain into surface pail veins. CNS is densely vascularises so neurones are mostly close to a capillary.
Neural factors
Sympathetic nerve stimulation to main cerebral arteries, reducing vasoconstriction; probably only operates when MABP is high.
Parasympathetic (facial nerve) stimulation producing slight vasodilation
Central cortical neurones relapsing a variety of vasoconstrictor neurotransmitters such as catecholamines
Dopaminergic neurones producing vasoconstriction (localised effect related to increased brain activity)
Innervation penetrating arteries and pericytes around capillaries. Pericytes are cells that wrap around capillaries, have diverse activities (immune function, transport properties, contractile)
May participate in the diversion of cerebral blood to areas of high activity.
Dopamine may cause contraction fo pericytes via aminergic and serotoninergic receptors.
The neural control on global brain blood flow is not well defined and its importance is uncertain.
Chemical factors
CO2 (direct) - vasodilator - small increase in pC)2 can give rise to a sharp increase in blood flow. Normal pCO2 = 40%
CO2 from blood or local metabolic activity generates H+ using carbonic anhydrase in surrounding neural tissue and in smooth muscle cells.
CO2 + H2O -> HCO3- + H+
H+ cant cross the BBB into smooth muscle.
Elevated H+ means decreased pH. This causes relaxation of the contractile smooth muscle cells, dilation of vessels, resulting in increased blood flow.
PH (i.e. H+, lactic acid .etc.) - vasodilator
Nitric oxide - vasodilator
K+ - vasodilator
Adenosine - vasodilator
Anoxia - vasodilator
Other (.e.g. kinins, prostaglandins, histamine, endothelins)
Local changes to cerebral blood flow allow imaging and mapping of brain activity using techniques such as PET scanning and functional MRI (fMRI).
In the CNS, increased blood flow equates to increased neuronal activity. More metabolically active, more CO2, more blood flow.
Describe cerebrospinal fluid.
CSF found in ventricular system and spinal canal into outer membrane of dura mater.
The ventricles, aqueducts and canals of the brain are lined with ependymal cells (epithelial-like glial cells, often ciliated). In some regions of the ventricles, this lining is modified to form branched villus structures: the choroid plexus.
CSF is produced by regions of choroid plexus in the cerebral ventricles:
Capillaries leaky but local ependymal cells have extensive tight junctions with lots of transporters it pump fluid across.
Secrete CSF into ventricles (lateral ventricles, 3rd ventricle via interventricular foramina, down cerebral aqueduct into 4th ventricle and into subarachnoid space via media and lateral apertures) - circulates
Volume: 80-150 ml
Functions: protection (physical and chemical), nutrition of neurones, transport of molecules
Composition of plasma and CSF (mM/L)
Diagram
CSF has little protein to prevent damage by plasma protein entering which can lead to infection.
Describe the blood-brain barrier.
A blood-brain barrier is needed because the activity of neurones is highly sensitive to the composition of local environment, the CNS midst be protected from the fluctuations in the composition of the blood. Homeostasis is key for brain. BBB is at level with CNS capillaries.
Exchange between blood and tissues occurs across capillary walls - continuous (moderately leaky), fenestrated - endocirne (leaky), sinusoid - liver, bone marrow (very leaky)
BBB: the capillaries of the CNS parenchyma derived from surface pail vessels. Vessel BBB properties increased in deeper vessels.
BBB capillaries have extensive tight junctions at the endothelial cell-cell contacts, massively reducing solute and fluid leak across the capillary wall.
Local environment causes vessels to become BBB like.
Differences between BBB and periphery capillaries:
Brain capillary is continuous with little transcultural vesicular transport. Interendothelial junctions are tight junctions.
Pericytes are closely approved to capillaries - maintain capillary integrity and functions. Periphery have sparse pericyte coverage whereas BBB have dense pericyte coverage.
BBB covered with “end-feet” from astrocytes whicha ew important for maintaining BBB properties.
Atrocytes in CNS can contact growth factors and other differentiation factors that cause vessels to become BBB like.
Hydrophilic solutes such as glucose, amino acids, antibiotics, some toxins cannot cross BBB due to tight junctions.
BBB controls the exchange of these substances using specific membrane transporters to transport into and out of CNS (influx and efflux transporters)
Blood-borne infectious agents may have reduced entry - CNS infections most commonly affect the meninges .e.g. meningitis
(Some evidence that loss of BBB can help with clearing some infections by allowing immune cells access)
Lipophilic molecules (O2, CO2, alcohol) cross the BBB via diffusion down connetration gradients.
Specific transport mechanisms for hydrophilic substances include:
- water, via aqua-or in (AQP1, AQP4) channels
- glucose, via GLUT1 transporter proteins
- amino acids, via 3 different transporters
- electrolytes, via specific transport systems
Some areas of the brain have capillaries lack BBB properties and are found close to ventricles and are called circumventricular organs (CVOs).
Capillaries are fenestrated. The ventricular ependymal lining close to these areas can be much tighter than in other areas, limiting exchange between them and CSF.
These regions are generally involved in secreting into the circulation or need to sample the plasma.
Eg.
Posterior pituitary and median eminence secrete bgromones
The area postrema samples the plasma for toxins and will induce vomiting
Other are involved in sensing electrolytes and regulate water intake
Explain the clinical importance of the BBB.
Describe the effect of antihistamines on BBB.
Describe how the BBB affects the treatment of Parkinson’s disease.
Trauma to CNS results in loss of BBB.
Pathological states such as inflammation, infection and stroke also lead to this.
Pharmacology issue - May want some drugs to access brain but cannot, others access brain too readily and cause adverse effects.
In treatment of allergy, H1 blockers are hydrophobic and can cross BBB by diffusion. Histamine is important in wakefulness and alertness so antihistamine made people drowsy. Nowadays, they’re used as sleep aids e.g. Nytol.
Second generation antihistamines are polar (have hydrophilic attachment) so do not readily cross BBB and cause drowsiness.
Dopamine cannot cross BBB so peripheral administration of dopamine cannot be used as Parkinson’s therapy. L-DOPA can cross BBB via an amino acid transporter and is converted to dopamine in brain however most circulating L-DOPA is converted to dopamine peripherally so less is available to access brain. Co-administration with the DOPA decarboxylase inhibitor, Carbidopa inhibits this conversion. It cannot cross BBB so does not affect the conversion in the brain.
Describe the structure of the thalamus.
The thalamus, subthalamus (subthalamic nucleus is target for deep brain stimulation in Parkinson’s; stop tremor through electrode) and hypothalamus are found in the diencephalon.
Hypothalamus is just beneath lateral ventricles and divided in middle by 3rd ventricle.
Thalamus sits ventral to the lateral ventricles and divided into 2 by 3rd ventricle.
Organised into discrete nuclei, nuclei refer to collection of neuronal cell bodies in CNS, ganglia in PNS, basal ganglia is exception in CNS.
Explain the functional significance of thalamic nuclei.
Relay site for numerous inputs and outputs (like Clapham J)
Key relay centre to cortical sensory areas
Involved in almost all sensory systems (except olfactory)
Enhances or restricts signals
Somatosensory pathway
Primary somatosensory cortex found behind central gyrus in parietal lobe.
To thalamus into gracile nucleus then cross over at second order neurone
Signal sent down dorsal column, input from dorsal root ganglion through dorsal horn of spinal cord.
Explain the relationship between intralaminar nuclei, reticular nucleus and reticular formation.
Intralaminar nuclei
Intralaminar nuclei project to various medial temporal lobe structures (e.g. amygdala (emotions, fear, anxiety; anterior temporal lobe), hippocampus (memory; behind amygdala at floor of temporal), basal ganglia (movement)
Mostly glutamatergic neruones (i.e. excitatory)
Loss of neurones in this region associated with progressive supranuclear palsy (rare brain disorder causing problems with walking and balance) and Parkinson’s disease
Reticular nucleus
Forms the outer covering of the thalamus.
Majority of neurones are GABAergic (e.g. inhibitory)
Unlike other thalamic nuclei, they don’t connect with distal regions but with other thalamic nuclei
Receive inputs from collaterals of their axons from thalamic nuclei therefore reticular nucleus acts to modulate thalamic activity (negative feedback).
Reticular formation
Set of interconnected pathways in the brainstem: send ascending projections to forebrain nuclei (ascending reticular activating system (ARAS))
Involved in consciousness and arousal: degrees of wakefulness depend on ARAS activity (increased activity = increased wakefulness)
Both intralaminar and reticular nucleus receive inputs from ARAS.
Recall functions of the hypothalamus and interactions with endocrine and autonomic systems in control of mood and behaviour.
Diagrams
Hypothalamus
Divided into two by 3rd ventricle
Collection of individual nuclei with distinct functions
Largely ipsilateral connections with other nuclei
Involved in 4 functions: fighting, fleeing, feeding, mating (fight or flight)
Function
Hypothalamus has direct connections with ANS
Connections with endocrine systems e.g. hypothalamic-pituitary axis
Control of behaviour e.g. feeding behaviour
Paraventricular nuclei send projections to ANS and posterior pituitary gland
PVN also involved in feeding behaviour
PVN lesions cause hyperplasia and weight gain
PVN receives input from hypothalamic uncle I involved in feeding
Suprachiasmatic nucleus (optic chiasm)
Circadian rhythm, sleep wave cycles
ANS connection via PVN
Also connected to pineal gland so controls secretion of melanin.
Lesions of SCN can cause disrupted sleep cycle
What is the brainstem?
Explain the development of the brainstem.
The part of the CNS, exclusive of the cerebellum, that lies between the cerebrum and the spinal cord.
The major divisions:
Medulla oblongata, pons, midbrain
Sulcus limitans - separates cranial nerve motor nuclei (medial) from sensory nuclei (lateral).
Diagram
Describe the diagrams of the brainstem.
From superior to inferior (Posterior)
Pineal gland: melatonin release, circadian rhythm, light-dark cycle
Superior colliculus: bump on back of brainstem, coordinated eye and neck movement
Inferior colliculus: protective auditory reflex (loud bang heard, should I leave or stay)
Trochlear nerve: only cranial nerve that emerges from back of the brainstem, supplies superior oblique muscle. Abducts, depresses eye.
4th ventricle: floor of 4th ventricle is back of the pons
Dorsal columns: gracile = medial, from leg
Cuneate = lateral, arms
Everything is bilateral in brainstem except pineal gland on roof of brainstem
Anteroinferior view
Superior to inferior
First 2 cranial nerves don’t emerge from brainstem, all neurones pass through cribriform plate of ethmoid bone to olfactory bulb. Olfactory - sense of smell, optic - light to retina to image
Optic chiasm
Pituitary stalk (infundibulum) immediately behind OC.
Mammillary body: base of hypothalamus
Cerebral peduncle: main sensory and motor tracts
Oculomotor nerve: eye movement, also autonomic functions e.g. constriction
Trigeminal nerve: sensory nerve of head and neck. Only one that emerges entirely from pons,3 divisions - touch+sensation, small root - motor function (chewing, mastication)
Abducens, facial, vestibulocochlear nerve: controls lateral rectus - outward gaze, facial expression, sound + expression.
Pyramids: cerebral peduncle emerges as pyramids.
Motor problem: corticospinal tract = pyramidal symptoms, cerebellar/other = extra pyramidal symptoms
Glossopharyngeal, vagus and accessory nerve: tongue and pharynx, parasympathetic, shoulder muscle - sternocleidomastoid and trapezius
Hypoglossal: under tongue, supplies muscles of tongue
Pyramidal decussation: contralateral motor control, cross over at base of medulla.
External structures: cerebral peduncle, pyramid, pyramidal decussation
Name all the cranial nerves in order.
Name all the key cranial foramina.
Name all the contents of these foramina.
Stylomastoid foramen: facial nerve (7) exit, vertebral arteries, anterior and posterior spinal arteries
Cribriform plate: olfactory nerve (1)
Optic canal: optic nerve (2), ophthalmic artery
Superior orbital fissure: oculomotor (3), trochlear (4), ophthalmic branch of trigeminal (5), abducens (6), superior ophthalmic vein
Foramen rotundum: maxillary branch of trigeminal (5)
Foramen ovale: mandibular branch of trigeminal (5)
Foramen spinosum: middle meningeal artery
Carotid canal: internal carotid artery
Internal acoustic meatus: facial (7) entry, vestibulocochlear (8), labyrinthine artery
Jugular foramen: glossopharyngeal (9), vagus (10), accessory (11)
Hypoglossal canal: hypoglossal (12)
Sigmoid sinus: internal jugular vein
Foramen magnum: spinal fibres of accessory (11), inferior medulla
What is the functional classification of spinal nerves?
What is the functional classification of cranial nerves?
Spinal nerves and cranial nerves
General somatic afferent (GSA): sensation from skin and mucous membranes
General visceral afferent (GVA): sensation from GI tract, heart, vessels and lungs
General somatic efferent (GSE): muscles for eye and tongue movements
General visceral efferent (GVE): preganglionic parasympathetic
Cranial nerves
Special somatic afferent
Vision, hearing and equilibrium
Special visceral afferent
Smell and taste
Special visceral efferent - only related to head and neck
Muscles involved in chewing, facial expression, swallowing, vocal sounds and turning head
Describe the cranial nerve nuclei.
Diagram
Describe the internal structure of the brainstem.
Diagram
Describe different brainstem pathology.
Lateral medullary syndrome;
Thrombosis of vertebral artery of PICA (posterior inferior cerebellar artery) - ischaemia
- vertigo (vestibular nuclei)
- ipsilateral cerebellar ataxia (unsteady of feet) (inferior cerebellar peduncle - inf coming from musculature to cerebellum - loss of balance/gait)
- ipsilateral loss of pain/ thermal sense (face) (spinal nucleus (trigeminal))
- horner’s syndrome - loss of sympathetic control, droopy eyelid (sympathetic tract - upper brainstem, loss of sympathetic innervation of eye area)
- hoarseness, difficulty swallowing (Nucleus ambiguus - musculature of throat)
- contralateral loss of pain/ thermal sense (trunk and limbs) (spinothalamic tract)
List and define the major somatosensory modalities.
Classify the sensory neurones.
A modality is a type of stimulus.
Modalities have specialised receptors, which will transmit info through specific anatomical pathways to brain.
Sensory nerve endings (axons) are specific to different modalities.
Touch/ pressure/ vibration —> mechanoreceptor (proprioception )(enclosed nerve endings: mechanoreceptors)
Temp —> thermoreceptor (free nerve endings: thermoreceptors and nociceptors)
Nociception —> nociceptor (pain)
Classification of sensory neurones:
Alpha beta-fibres: innocuous (not harmful) mechanical simulation (large and myelinated therefore fast)
E.g. Merkel cells (light touch and superficial pressure), Pacinian corpuscle (detects deep pressure, high frequency vibration and tickling)
Alpha delta-fibres: noxious (harmful) mechanical and thermal stimulation (less fast)
C-fibres: noxious mechanical and thermal and chemical stimulation (no myelinated, slower, achy pain)
Define the terms: receptor, stimulus threshold, stimulus intensity, adaptation, receptive field, 2 point discrimination and lateral inhibition.
Receptors are transducers that convert energy from the environment into neuronal action potentials.
A threshold is the point of intensity at which the person can just detect the presence of a stimulus 50% of the time = absolute threshold
Need a stimulus to be strong enough to send a.p. (generator potential to action potential)
Adaptation: tonic receptors
Detect continuous stimulus strength
Continue to transmit impulses to the brain as long the stimulus is present, keeps the brain constantly informed e.g. Merkel cells - slowly adapt allowing for superficial and fine touch to be perceived (stroking)
Adaptation: - phasic receptors
Detect a change in stimulus strength
Transmit an impulse at the start and the end of the stimulus e.g. Pacinian receptor - sudden pressure excites receptor, transmits a signal again when pressure is released
The receptive field is the region on the skin which causes activation of a single sensory neurone when activated.
- Small receptive fields allow for the detection of fine detail over a small area - precise perception e.g. fingers have many densely packed mechanoreceptors with small receptive fields
- Large receptive fields allow the cell to detect changes over a wide area (less precise perception)
Two point discrimination is the minimum distance at which two points are perceived as separated. Related to the size of the receptive field. (Smaller, more denser)
Quantity sensory testing used to test sensitivity (13 tests) can be used for pain e.g. brush.
Lateral inhibition: a receptive field can overlap with another receptive field.
Difficult to distinguish between 2 stimulus fields.
Lateral inhibition prevents the overlap of receptive fields.
Facilitates pinpoint accuracy in localisation of the stimulus.
Mediated by inhibitory interneurones within dorsal horn of spinal cord.
Facilitates enhanced sensory perception (discrimination)
The difference between adjacent inputs is enhanced by lateral inhibition.
Lateral inhibition is the process by which stimulated neurons inhibit the activity of nearby neurons. Prevents spreading in lateral direction.
Describe nociceptors and pain pathways.
Alpha delta fibres mediate sharp, intense or first pain
Type 1: noxious mechanical
Type 2: noxious heat
C fibres mediate dull, aching or second pain
Noxious thermal, mechanical and chemical stimuli (polymodal)
Lateral spinothalamic tract (sensory component) Spinoreticular tract (emotional) Peripheral sensitisation (decrease thresholds to peripheral stimuli at the site of injury) Central sensitisation (decrease thresholds to peripheral stimuli at an adjacent site to the injury, expansion of receptive field, spontaneous pain)
Explain the gate control theory.
Inhibition of primary afferent inputs before they are transmitted to the brain through ascending pathways.
Activation of alpha beta fibres activates inhibitory interneurones to block projection neurones activated by c-fibres .e.g. rubbing to reduce pain
Describe the touch and proprioception pathway.
Alpha beta fibres enter via the dorsal horn and enter the dorsal column pathways.
Information conveyed from lower limbs and body (below T6) travel ipsilaterally along the gracile tract.
Information conveyed from upper limbs and body (above T6) travel ipsilaterally along the cuneate tract.
1st Oder neurones terminate in the medulla:
Fibres in the gracile tract have their first synapse in the gracile nucleus.
Fibres in the cuneate tract have their first synapse in the cuneate nucleus.
2nd order neurones cross in the medulla:
Second order axons decussate (cross the midline) in the caudal medulla
Forms the contralateral medial lemniscus tract.
2nd order neurones terminate in the thalamus:
The axons terminate in the ventral posterior lateral nucleus of the thalamus (VPL)
3rd order neurones terminate in the somatosensory cortex:
3rd order neurones from the VPL project to the somatosensory cortex.
Size of the somatotopic areas is proportional to density of sensory receptors in that body region (somatosensory homunculus)
Pain and temperature location not as precise
Describe the pain, temperature and crude touch pathway.
Spinothalamic (anterolateral) pathway
Pain and temperature sensations ascend within the lateral spinothalamic tract
Crude touch ascends within the anterior spinothalamic tract
1st order neruones terminate in the dorsal horn:
Primary afferent axons terminate upon entering the spinal cord.
Second order neurones decussate immediately in the spinal cord and form the spinothalamic tract.
2nd order neurones terminate in the thalamus:
2nd order neurones terminate int he ventral posterior lateral (VPL) nucleus of the thalamus
Explain anterior spinal cord lesion.
Blocked anterior spinal artery causes ischaemic damage to the anterior part of the spinal cord.
Spinothalamic tract damage causes pain and temperature loss below the level of the lesion.
Retained light touch, vibration and 2 point discrimination due to intact dorsal columns.
Describe pain.
An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.
Neuropathic pain: pain caused by a lesion or disease of somatosensory nervous system .e.g. diabetic, sciatica, trauma, post-surgical, chemotherapy
Pain in area of neurological dysfunction
Sharp burning electric shocks
Poor response to usual analgesic drugs .eg. Opiates
Nociceptive: noxious stimulation of a nociceptor (somatic or viscera) e.g. skin, muscles, joints, bones
Alloy is: pain due to a stimulus that does not normally provoke pain e.g. brush
Hyperalgesia: increased pain from a stimulus that normally provokes pain
Primary hyperalgesia describes pain sensitivity that occurs directly in the damaged tissues. Secondary hyperalgesia describes pain sensitivity that occurs in surrounding undamaged tissues.
Sensitisation: increased responsiveness of nociceptive neurones to their normal input.
Hypoalgesia: diminished pain in response to a normally painful stimulus.
Parathesia: abnormal sensation whether spontaneous/ evoked.
Describe descending control pathways.
Describe ways you can target descending control systems for paint relief.
Facilitation and inhibition of nociceptive processing in the dorsal horn.
The periaqueductal gray (PAG, also known as the central gray) is a nucleus that plays a critical role in autonomic function, motivated behavior and behavioural responses to threatening stimuli.
Monoamines:
Serotonin (facilitate - harmful)
Noradrenaline (inhibits - protective)
Pain relief:
Opioids (endogenous and exogenous) inhibit pain. Reduce pain transmission in dorsal horn by inhibiting glutamate release .i.e. activation of spinothalamic neurones.
Antidepressants: TCA, SNRI, SSRI - target adrenaline
Define functional segregation and hierarchical organisation.
Functional segregation: motor system organised in a number of different areas that control different aspects of movement.
Hierarchical organisation: high order areas of hierarchy are involved in more complex tasks (programme and decide on movements, coordinate muscle activity) - more than one muscular system coordinated
Lower level areas of hierarchy perform lower level tasks (execution of movement) - carry out instructions
Explain the primary motor cortex (M1)
Location: Precentral gyrus, anterior to central sulcus in frontal lobe.
Function: control fine, discrete, precise voluntary movement
Receives info from other cortical areas and sends descending signals to thalamus and brainstem to execute movement.
There’s a somatotopic organisation - Penfield’s motro homunculus
Explain the descending motor pathways.
Primary motor cortex contain Betz cells (pyramidial cells - neurones) -> fibres pass through internal capsule of basal ganglia -> cerebral penducle in midbrain -> pass through pons into pyramids -> cross over - decussation at bottom of medulla -> descend through corticospinal tract -> project to ventral root of spinal cord at appropriate level and synapse with lower motor neurones (alpha neurones) -> project out to musculature through VR?? By spinal nerves.
Remaining 5-10% of fibres don’t cross at medulla, stay ipsilateral and descend in anterior corticospinal tract. Decussation happens at level of spinal cord. Largely input to thorax, intercostal muscles, axial musculature.
Explain the corticobulbar pathways.
Referring to motor neurones in brainstem - cranial nerve nuclei.
The corticobulbar tract is a two-neuron path which unites the cerebral cortex with the cranial nerve nuclei in the brainstem involved in motor functions (apart from the oculomotor nerve).
