Neuroanatomy Flashcards

1
Q

Name and describe disorders of myelination.

A

Hypomyelination – disorders resulting in diminished amounts of myelin within the sheath.

Dysmyelination – disorders resulting in malformations or defects in the myelin sheaths.

Demyelination – disorders causing damage to pre-existing normal myelin. An example in humans in the autoimmune disease multiple sclerosis, where the body amounts an immune response to the myelin, causing it to be damaged/destroyed.

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2
Q

What are some examples of myelin sheath disorders in animals?

A
  • Canine distemper virus
  • Visna – another viral condition found mainly in sheep, of which the neurological form is called Visna
  • Poisoning with pesticides – for example, organophosphates
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3
Q

What are the clinical signs of myelin disorders?

A
  • Whole body tremor across all body regions, especially on exertion.
  • Motor signs such as weakness or power loss in the limbs
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4
Q

What does the number of poles in a neurone refer to?

A

Refers to the number of processes (axon/dendrites) coming off of the neurone cell body. Unipolar is one, bipolar is two, multipolar is three or more.

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5
Q

What are pseudo unipolar neurones?

A

Are general somatic afferents - they arise from the periphery, such as skin/muscles, and project to the CNS with their cell bodies in the dorsal root ganglion of the spinal dorsal root.

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6
Q

What is an example of bipolar neurones?

A

With two poles (one dendrite and one axon), found in the retina

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7
Q

Which types of neurone are multipolar neurones?

A

Motor

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8
Q

What is multiple sclerosis?

A

White matter is myelinated. In humans, multiple sclerosis is autoimmune attack of myelin sheaths.

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9
Q

Describe how spinal nerves arrive from the periphery and into the CNS and brain.

A
  • Spinal nerves are mixed at this level and then when they reach the spinal cord, they divide into dorsal and ventral branches.
  • Dorsal root is sensory only and ventral root is motor only.
  • A dorsal root ganglion is a group of mixed nerve cell bodies.
  • Ventral root contains somatic and autonomic neurones, going to skeletal muscle and smooth and cardiac muscle respectively.
  • Can get interneurons that bridge between motor and sensory.
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10
Q

Briefly distinguish the central and peripheral nervous systems.

A

CNS – brain and spinal cord. Protected by skull and spinal column

PNS – cranial and spinal nerves. Unprotected.

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11
Q

Distinguish the sensory and motor divisions of the peripheral nervous system.

A

Sensory division
- Somatic
- Visceral

Motor division
- Somatic – somatic tissues from somites, skin and skeletal muscle
- Autonomic – autonomic tissues are ‘self-governing’: cardiac muscle, smooth muscle, glands

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12
Q

Distinguish the sympathetic and parasympathetic divisions of the autonomic nervous system.

A

Sympathetic – sight or flight

Parasympathetic – rest and digest

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13
Q

How can nerves be classed?

A

Sensory and motor nerves can be classified according to their distribution.

Afferent = sensory
Efferent = motor

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14
Q

Name and describe the 4 categories of general/widely distributed nerves.

A

General somatic afferent – touch, temperature, pain from non-visceral structures

General somatic efferent – motor to skeletal muscle

General visceral afferent – distension, temperature, pain, chemical concentrations from viscera

General visceral efferent – motor to viscera, smooth muscles, cardiac muscle and glands

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15
Q

Name and describe the 3 categories of special/location restricted nerves.

A

Special somatic afferent – vision, hearing and balance

Special visceral afferent – taste and olfaction

Special visceral efferent/ branchiomotor – muscles of branchial arches derived from the embryo

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16
Q

Describe the features and properties of grey matter.

A
  • Nuclei – aggregations of neurone cell bodies in the brain
  • Ganglia – aggregations of nerve cell bodies in the peripheral nervous system
  • Unmyelinated axons
  • Appears white in stain
  • Referred to nucleus in CNS and ganglia in PNS
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17
Q

Describe the features and properties of white matter.

A
  • Funiculi/columns – white matter in the spinal cord consisting of fasciculi
  • Fasciculi/tracts – axons of the same origin, destination and function
  • Fasciculus divided into individual fasciculi
  • Myelinated axons
  • Appears grey in stain
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18
Q

Where does the CNS develop from?

A

Ectoderm

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19
Q

How does the neural tube form in CNS development?

A

Ectoderm has a layer of cells/neural plate folds inwards around notochord and fold inwards so the 2 sides come together forming a closed tube above the notochord. Neural crest cells can become adrenal medulla cells, odontoblasts and ganglia, among others. There is detachment of neural plate from ectoderm and forms a layer over the neural tube.

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20
Q

What occurs if the neural tube fails to close rostrally?

A

Anencephaly. Cell not formed, cranioneural pore fails to close and neural contents exposed.

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21
Q

Describe anencephaly.

A
  • Forebrain structures arising from the most rostral regions of the neural tube fail to form.
  • These support the growth of the associated skull vault, so may trigger abnormalities here.
  • Cardiorespiratory centres are intact and functioning but this malformation in incompatible with thus and so young may survive but die soon afterwards.
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22
Q

What occurs if the neural tube fails to close caudally?

A

Spina bifida/dermoid sinus. Embryological sinus that forms a connection between the skin and the nervous system, leading to frequent infections.

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23
Q

Describe spina bifida.

A
  • Leads to failure of surrounding tissue that form the vertebral arches t meet in the midline and fuse.
  • Leads to nervous tissue being exposed or merely protected/covered over with just skin and subcutaneous tissue (spina bifida occulata)
  • Cystic swellings which herniate through the skin can also form – spina bifida cystica, the more severe form of the disease, causing infection and neurological complications.
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24
Q

Describe a dermoid sinus.

A

An embryological tissue remnant which may be seen more commonly in certain species such as the Rhodesian Ridgeback.

  • Arises as a result of the neuroectoderm tissue of the neural tube failing to detach away from the overlying ectoderm cells, which will go on to form skin.
  • Usually resembles a tube itself, like spaghetti.
  • Since the neural tube spans the length of the embryo’s back, the defect may be located anywhere but is most commonly in the cervical or upper thoracic regions.
  • Extent of the communication between skin and spine varies. If deep and to meninges, can cause infections and meningitis.
  • Seen in other species: rhodesian ridgebacks, kerry blues, boxers and shih tzus. Affected individuals should not be bred.
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25
Q

What are the 3 primitive brain vesicles and how do they form?

A

Rostral end becomes the brain and 3 primitive brain vesicles develop:

  • Forebrain/prosencephalon
  • Midbrain/mesencephalon
  • Hindbrain/rhombencephalon, due to diamond shape of 4th ventricle found here. Cerebellum, pons and medulla are the main structures.
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26
Q

What does the caudal end of the neural tube become?

A

Spinal cord

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27
Q

Name and describe the 2 adult derivatives/subdivisions in the forebrain.

A

Telencephalon/cerebrum – cerebral hemisphere and basal nuclei, lumen and lateral ventricle

Diencephalon – thalamus, hypothalamus, epithalamus, subthalamus, lumen, lateral ventricle

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28
Q

Name the structures of the telencephalon.

A

Cerebral cortex
Hippocampus
Lateral ventricle
Basal nuclei

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29
Q

Name the structures of the diencephalon.

A

Thalamus
Hypothalamus
3rd ventricle
Interthalamic adhesion

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30
Q

What is the adult derivative of the midbrain and its structures?

A

Mesencephalon:

Tectum – roof
Tegmentum – floor
Lumen – midbrain/cerebral aqueduct

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31
Q

What are the 2 adult derivatives/subdivisions of the hindbrain/rhombencephalon?

A

Metencephalon – pons and cerebellum

Myelencephalon – medulla oblongata

Also has 4th ventricle that is diamond shaped.

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32
Q

Describe the species differences in the cerebellum.

A

Regulates movement so the ratio of cerebrum : cerebellum is smaller in animals with complicated gait cycles (cerebellum larger in animals with complicated gait cycles, like horses)

Dog = 8:1
Horse = 7:1
Man = 9:1

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33
Q

What are cerebellar disorders?

A

Disorders result in ataxia (incoordination) – motor, sensory and vestibular.

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34
Q

What are the major features of the spinal cord?

A
  • Cervical intumescence/enlargement/swelling
  • Lumber intumescence/enlargement/swelling
  • These are to do with limb access
  • Spinal cord tapers to conus medullaris
  • Cauda equina – plexus like structure of nerves
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35
Q

What is the structure of the brainstem?

A

Brain stem is a stalk like structure coming off the caudal end of the brain and is separate from the hindbrain.

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36
Q

What is cranial shift of the spinal cord and why it occurs?

A

There is cranial shift of spinal cord segments, as spinal vertebrae/column grows faster than the spinal cord, which has significant clinical consequences: in the dog, segments L5-S3 lie between vertebrae L4-L5, this a disc protrusion at this level has grave consequences.

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37
Q

In the dog, what is the consequences of cranial shift?

A
  • L5-S3 regions of the cord will lie at the level of L4-5 vertebrae.
  • If there is localised compression of this region of the cord by a prolapsed disc, then the consequences will be potentially catastrophic.
  • L5-S3 segments give rise to the spinal nerves which supply the hindlimbs and the pudendal regions.
  • If there is irreparable damage to these neurones then the animal hindlimbs will be paralysed and they will also lose the important autonomic and somatic control to their perineum and pelvic viscera, making them incontinent.
  • This syndrome may also be generated by compression of the cauda equina nerves, called cauda equina syndrome.
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38
Q

Describe the structure of a transverse section through the spinal cord.

A
  • Central canal contains CSF, an ultrafilatrated plasma that nourishes nervous tissue and has protective features, and is a continuation of the ventricle system.
  • Dorsal median fissure shallower than ventral median fissure.
  • Dorsal, lateral and ventral funiculi of white matter and dorsal and ventral horns of grey matter, lateral/intermediate in thoracolumbar areas too (contains sympathetic fibres).
  • Filum terminale tethers spinal cord to end of vertebrae.
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39
Q

How do transverse sections vary through the spinal cord?

A

Ventral horns large in lower cervical, lumbar and sacral, as they contain cell bodies of motor neurones. Lateral/intermediate horns in thoracic region and is the smallest.

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40
Q

Describe the canine lobes of the brain.

A
  • Canine has large olfactory lobe.
  • Lead back to piriform lobes, heavily implicated in small due to close proximity to olfactory lobe.
  • Occipital lobe at back of brain is implicated in sight.
  • Auditory cortex in temporal lobe.
  • Motor cortex spread around cruciate sulcus.
  • Sensory cortex behind cruciate sulcus.
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41
Q

Which imaging can be used to view the brain and spinal cord.

A

Not visible on radiographs, unless a contrast medium is injected into the subarachnoid space.

Myelography
CT
MRI

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42
Q

What are the 3 main arteries supplying the brain?

A

Rostral cerebral artery = medial hemisphere

Middle cerebral artery = lateral and ventral hemisphere

Caudal cerebral artery = occipital lobes

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43
Q

List the arteries of the circle of willis.

A

Ventral spinal
Vertebral
Basilar
Caudal cerebellar
Rostral cerebellar
Caudal communicating
Internal carotid
Caudal cerebral
Middle cerebral
Rostral cerebral
Rostral communicating

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44
Q

How are there rostral and caudal circulations?

A

If big vessel gets blocked, there is no other pathway often. If smaller arteries are blocked, there may be an alternative pathway.

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45
Q

How are there rostral and caudal circulations?

A

If big vessel gets blocked, there is no other pathway often. If smaller arteries are blocked, there may be an alternative pathway.

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46
Q

What is cerebrospinal nematodiasis?

A

Animals that are not wormed with Ivermectin are at risk from embolisms from lesions in walls of larger blood vessels induced by worms.

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47
Q

What occurs in cerebrospinal nematodiasis?

A
  • The larvae trigger an encephalitis – inflammation of the parenchyma of the brain.
  • Inflammatory reaction to the invasion can also cause arteries, such as inflammation of the vessel wall.
  • This triggers formation of both aneurysms and thrombi in the lumen of the vessel.
  • These can trigger cerebral infarction, in which parts of the brain die off/undergo necrosis as a result of being deprived of their blood supply.
  • Brain tissue is very active and has a high metabolic demand from its blood supply.
  • Any loss, even fleeting, can lead to rapid onset, irreversible damage.
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48
Q

How is loss of neuronal population shown?

A

Reflected in narrowing of the folial white matter.

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49
Q

What is the issue with blood supply to the ox brain during slaughter.

A
  • Proximal 2/3 of internal carotid artery is occluded by 18 months of age
  • There is an anastomosis between the maxillary artery and the internal carotid artery
  • Most importantly, there is a vertebromaxillary anastomosis.
  • There is continued perfusion to the brain when ICA is cut in halal slaughter.
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50
Q

Describe the venous drainage of the brain.

A
  1. Dorsal and ventral sagittal sinuses receive cerebrospinal fluid via arachnoid granulations as well as blood.
  2. Straight sinus
  3. Transverse sinus
  4. Eventually drain to maxillary vein
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51
Q

What is the blood brain barrier and its function?

A
  • Nonfenestrated endothelial cells joined by tight junctions
  • Thick basement membrane
  • Complete layer of astrocyte foot processes on the basement membrane
  • Protects and controls the neural environment
  • Essential to toxic metabolites and bacteria not getting to the brain
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52
Q

What is the clinical relevance of Ivermectin to the blood brain barrier?

A

Ivermectin toxicity. To treat meningitis, vets must consider which broad spectrum antibiotic can cross the blood brain barrier and whether the animal is to enter the food chain or not.

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53
Q

What are the causes of hydrocephalus?

A

A blockage of the CSF circulation.

An example, would be a tumour in the midbrain, obstructing the cerebral aqueduct which runs through it.

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54
Q

Where could hydrocephalus blockages occur?

A

Anywhere along flow route, although small diameter structures, due to their size, are more prone to causing such issues, such as:

  • Interventricular foramina
  • Cerebral aqueduct
  • Apertures which allow CSF to perforate out of the ventricular system and run in the subarachnoid space
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55
Q

What occurs in hydrocephalus?

A
  • A disorder which arises from abnormal circulation of the cerebrospinal fluid from the ventricular system.
  • Grossly speaking, it is a factor of either abnormalities in the production or drainage of the CSF.
  • Fluid unable to drain proximal to the site of blockage so both fluid and pressure will develop on the brain, compressing the nervous tissue and causing the ventricular spaces to enlarge. (Cavalier King Charles Spaniels and other brachycephalic breeds)
  • Congenital, usually a result of a structural neurological abnormality related to embryological development.
  • Acquired, of which tumour account for most common causes
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56
Q

What is the role of the cerebellum?

A

Cerebellum is immensely important as a fine tuner of movements initiated by the motor system – both pyramidal and extrapyramidal systems. Cerebellum is sensitive to incoming sensory information from the body and generates outputs which feed into those arising from other motor systems, refining their outcomes based on the information it has been privy to.

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57
Q

What are the possible symptoms in animals with cerebellar dysfunction?

A

Ataxia
Spasticity
Hypermetria
Tremor

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58
Q

Describe ataxia.

A
  • Abnormal co-ordination of movement.
  • Thus may be seen in any body region and arises as a result of the important sensory inputs to the cerebellum being lost, such as damage to the ascending tracts, or damage to the integrative cerebellar centre which processes the information.
  • If the cerebellum cannot process proprioceptive information regarding the position of the limbs, head, trunk, etc.
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59
Q

Describe spasticity.

A

Loss of inhibitory cerebellar function to fine tune motor control lead to increased tone within muscles.

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60
Q

Describe hypermetria.

A

An overshooting movement of the limbs or grossllu amplified stepping movements (goose stepping)

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61
Q

Describe tremors.

A

Postural shaking/instability from failure to balance activities of opposing muscle groups, such as flexors and tendons. A cerebellar tremor is an intention tremor, which is associated with an intended action.

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62
Q

What is vascular compromise of the cerebellar?

A

If there is vascular compromise to the cerebellum via 1 or more of its arteries becoming diseased, then cerebellar signs may become apparent. Main symptoms: spasticity, hypermetria, ataxia and tremor, without paresis.

Important vessel supplying the cerebellum include the rostral and caudal cerebellar arteries.

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63
Q

Which arteries give rise to the circle of willis?

A

Internal carotid artery – supplying the rostral regions of the brain

Basilar artery – arising form the paired vertebral arteries, supplying the caudal regions of the brain.

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64
Q

What are the species differences in the circle of willis?

A
  • Circle of willis can also be supplied with blood via anastomoses form the maxillary artery, which is a branch of the external carotid artery. This is a significant supply in cats and sheep in which the proximal 2 3rds of the internal carotid artery obliterates in the adult, meaning that the blood supply needs to be derived from another source. The maxillary artery supplies the vast majority of the blood to the circle of willis in these species.
  • In the ox, the proximal 2 3rds of the internal carotid artery is absent, requiring an arterial source from another vessel. These arise from both the maxillary artery and vertebral arteries, at the vertebromaxillary anastomosis. This means if both the maxillary and vertebral arteries, each supply a significant amount of blood to the arterial circle in the ox.
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65
Q

How does species variation in the circle of willis have implications on slaughter?

A
  • The throat cut will halt the blood supply from the common carotid artery on its way to the brain and so the animal will die as a result of exsanguination and brain death.
  • This does not lesion the vertebral arteries, which arise from subclavian arteries and ascend in the transverse foramina of the cervical vertebra, protected along their length.
  • Any animal intended for slaughter with a significant vertebral blood supply to the brain, such as the ox, may retain the capacity to preserve the blood supply to their brain for longer and so remain conscious for longer.
  • This is overcome, as is the pain from throat cutting and exsanguinating by the practice of stunning the animal first of all.
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66
Q

List the subcortical structures.

A
  • Basal nuclei
  • Thalamus
  • Hypothalamus
  • Limbic system – associated with memory and emotion
  • Midbrain
  • Pons
  • Medulla oblongata
  • Cerebellum
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67
Q

What are the basal nuclei?

A

These are areas of grey matter (unmyelinated) in the telencephalon.

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68
Q

What are the roles of the basal nuclei?

A
  • Control of voluntary movement
  • Procedural learning (through a series of different steps)
  • Eye movement
  • Cognition
  • Emotion
  • Use the neurotransmitter, dopamine
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69
Q

What do lesions of the basal nuclei cause?

A

Lesions of the basal nuclei cause dyskinesia and increased muscle tone when substantia nigra is affected (Parkinson’s in humans).

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70
Q

What makes up the basal nuclei?

A

Caudate nucleus
Putamen (more lateral) is bilateral
Globus pallidus (more medial)

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71
Q

Describe the structure of the thalamus.

A
  • Arises from diencephalon.
  • Bilateral with the 3rd ventricle running between the 2.
  • They are joined by the interthalamic adhesion.
  • Grey matter structure with lots of nuclei.
  • Lateral ventricles drain into the midline/3rd ventricle.
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72
Q

What are the roles of the thalamus?

A
  • Relay to and from cerebral cortex. No relay from olfactory cortex
  • Processing of sensations – touch, pain, proprioception
  • Consciousness
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73
Q

What are the roles of the hypothalamus?

A
  • Autonomic control – via connections with the reticular formation.
  • Appetite, thirst, temperature, electrolyte and water balance (homeostasis)
  • Sleep
  • Behaviour
  • Control of pituitary
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74
Q

What are the clinical relevances of the hypothalamus?

A

Damage to the hypothalamus can occur due to fractures, tumours or infections. Various effects including behavioural changes and alimentary disorder.

Anterior lobe of pituitary gland prone to tumours, can compress the optic chiasma and cause blindness.

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75
Q

What are the symptoms of the lesions of the diencephalon?

A
  • Abnormal behaviour
  • Total body hypalgesia (decreased pain sense)
  • Slow postural reactions
  • Depression leading to progressive steps ending in coma (ARAS)
  • Blindness
  • Alterations in thermoregulation and thirst, etc
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76
Q

What are the forebrain structures associated with the limbic system?

A

Hippocampus
Amygdala and piriform lobe
Septal nuclei
Cingulate gyrus
Hypothalamus
Thalamus

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77
Q

What are the associated roles of the limbic system?

A

Emotion
Memory
Learning
Personality
Behaviour

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78
Q

Describe the structure of the hippocampus.

A
  • Gives rise to axons forming the fornix (arch)– run to mammillary bodies of the hypothalamus
  • Interlocking C shape apparent in cross section
  • Mid-sagittal section needed to see in more detail. Embedded deep in the walls of the cerebral hemisphere.
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79
Q

What is the corpus callosum?

A

Series of fibres that allow right and left hemispheres to communicate.

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80
Q

What is the cingulate gyrus?

A

Forms a belt over the top of the corpus callosum

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81
Q

What is the amygdala?

A

Almond shaped and is part of the limbic system.

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82
Q

What is the septal nuclei?

A

Within septum pellucidum rostrally. Divides the 2 lateral ventricles.

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83
Q

What is the hallmark of the midbrain?

A

Hallmark of midbrain is the cerebral aqueduct that runs through it.

Tectum - everything dorsal to the plane of the cerebral aqueduct.

Tegmentum - everything ventral to the cerebral aqueduct.

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84
Q

Describe the structure and function of the tectum.

A

Rostral and caudal colliculi – corpora quadrigemina. 4 swellings, each called colliculi, rostral involved in visual processing and caudal one involved in auditory processing.

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85
Q

Describe the structure and functions of the tegmentum.

A
  • Crus cerebri
  • Cerebral peduncles
  • Substantia nigra – black substance
  • Red nucleus
  • Parasympathetic and motor nuclei of CNIII
  • Motor nucleus of CNIV
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86
Q

What does trochlear nerve control?

A

CNIV controls on ocular muscle and ocular nerve controls the rest of the ocular muscles, which allow to change gaze.

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87
Q

What is the role of the parasympathetic nucleus?

A

Parasympathetic nucleus has neurones heading for the iris and pupillary muscles.

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88
Q

What is the role of the red nucleus?

A
  • Start of rubrospinal tract
  • Vital for control of posture and movement
  • Well developed in domestic species compares to corticospinal tract in humans and primates
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89
Q

What are the roles of the reticular formation?

A
  • Runs throughout brainstem
  • Alerts the cerebral cortex to maintain wakefulness (ARAS)
  • In the pons and medulla, regulates visceral functions and stimulate or inhibit motor activity of body and limbs.
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90
Q

What is the crus cerebri?

A

Involved in transmission of motor tracts to and from the higher areas of the brain, such as the cortex.

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91
Q

What are the symptoms caused by disorders affecting the midbrain?

A
  • Depression, leading to coma (ARAS)
  • Ataxia – red nucleus and substantia nigra
  • Stiffness with reduced voluntary function of muscles, spastic tetraparesis – red nucleus and substantia nigra
  • Hypalgesia – crus cerebri/tegmentum
  • Deviation of eye (strabismus) – general somatic efferent of III and IV
  • Dilation of pupil – general ventral efferent of III
92
Q

Describe the structure of the reticular formation in the pons.

A
  • Upper motor neurone control of cardiovascular and respiratory centres, swallowing, vomiting, etc.
  • Ascending reticular activating system.
  • Oldest part of motor system is the reticulospinal tracts
  • Also, pontine fibres that cross left to right.
93
Q

Which nerve nucleus comes off the pons?

A

Trigeminal

94
Q

Describe what the reticular formation in the medulla oblongata integrates with.

A

Cardiovascular control
Autonomic regulation
Medullary reticulospinal tracts

95
Q

Which nerve nuclei come off the medulla oblongata?

A

Nuclei of CNVI-XII come off the medulla.

96
Q

What are the medullary pyramids and their functions?

A

Contains corticospinal fibres of the pyramidal tract, controls voluntary movement of mainly distal muscle of a limb.

97
Q

Which nerves arise from the midbrain?

A

CNIII and CNIV arise form midbrain

98
Q

What is located on the ventral surface of the medulla oblongata?

A

Olivary nucleus – pre-processes input to the cerebellum.

Medullary pyramids on ventral surface. The olive is a bulbous structure found either side of the pyramids, involved in motor control due to its input to the cerebellum.

99
Q

Describe the structure of the cerebellum.

A
  • Has rostral lobe, caudal lobe and flocculonodular (oldest part of cerebellum) lobe.
  • Primary fissure is more rostral and caudo-lateral fissure.
  • Has 2 hemispheres.
  • Structure running straight down the middle is vermis.
  • Right hemisphere controls right side of the body and vice versa, unlike the cerebrum, in which the right hemisphere controls of the left side of the body and vice versa. - Grey matter outside and white matter inside.
  • There are little cerebellar nuclei within the white matter.
100
Q

What are the roles of the cerebellum?

A
  • Balance and posture
  • Fine motor control
  • Modifies intended movement
101
Q

What are the causes and clinical signs of cerebellar disease?

A

Caused by trauma, tumours, infarcts, viruses during pregnancy.

  • Ataxia in all legs
  • Wide based stance (to correct the ataxia)
  • Tremor
  • Loss of balance
102
Q

How is the cerebellum connected to the brainstem?

A

By peduncles. 3 per side:

Rostral CP– midbrain
Middle CP – pons
Caudal CP – medulla

103
Q

What is cerebellar abiotrophy?

A

An inherited condition in Arabian horses, many dog breeds and occasionally cattle.

104
Q

What are the starting points of clinical neurological assessment?

A
  1. Signalment
  2. History – acute vs chronic onset
  3. Observant – as animal enters room: mental status, behaviour, posture, movement and gait.
  4. General physical examination:
    - General body condition – muscle wastage
    - Demeanour – responsive to environment? depressed?
    - Orthopaedic vs neurological?
105
Q

What is needed for proper functions of mental status?

A
  • Cerebral cortex
  • Relay via thalamus
  • Ascending reticular activating system (ARAS)
  • Sensors of peripheral input
106
Q

What is the ascending reticular activating system?

A
  • Part of the reticular formation
  • Receives proprioceptive, exteroceptive and interoceptive afferents
  • Brainstem lesion can cause coma

Activates cortex:
- Smelling salts
- Shaking awake
- Water/slap in face
- Loud noise/bright lights

107
Q

What are the cornerstones of neurological examination?

A

Neurological reflexes and responses are the cornerstone of any neurological examination.

  • A reflex is an unconscious reaction to a stimulus
  • A response is a conscious reaction to a stimulus
108
Q

List the cranial nerves.

A

I = olfactory
II = optic
III = oculomotor
IV = trochlear
V = trigeminal
VI = abducent/abducens
VII = facial
VIII = vestibulocochlear
IX = glossopharyngeal
X = vagus
XI = accessory
XII = hypoglossal

109
Q

Describe the path of the olfactory nerve.

A
  1. Afferent fibres from the olfactory mucosa and vomeronasal organ contribute to CNI.
  2. Synapse in olfactory bulb. Most of fibres run in the olfactory tract.
  3. Can synapse in:
    - The olfactory tubercle – project to piriform cortex
    - Limbic system
    - Hypothalamus and brainstem reticular formation
110
Q

How is the olfactory nerve tested for?

A

Test nerve and pathway clinically by hiding a biscuit/treat in one hand and seeing if the dog can detect it. Difficult to confirm so is not always tested and subjective.

111
Q

What is the optic nerve involved in?

A
  • Visual pathway
  • Coordinating eye movements
  • Pupillary constriction
  • Reflex responses to visual stimuli
112
Q

Describe the visual pathway of the optic nerve.

A

Activating the rods and cones activates the bipolar cells. Optic nerves project back from retina and meet in middle at a cross called the optic chiasm. Allows for exchange of information between the 2 visual fields. Then to optic tracts which project back to the thalamus and then to the optic cortex.

113
Q

Describe the 3 neurones involved in the visual pathway.

A

Neurone 1 = bipolar cell of retina

Neurone 2 = retinal ganglion call, forms the optic nerve

Neurone 3 = for conscious perception of light. This is on the thalamus, lateral geniculate nucleus. Projects to occipital cortex via the internal capsule.

114
Q

What are visual reflexes?

A

Information comes in to form vision but output to the eye must occur for management of the vision. Conveyed by oculomotor and trochlear nerves.

  • 20% of axons of the optic nerve run to the midbrain, where visual reflexes are integrated.
  • Controlling reflex response to bright light (PLR)
  • Coordinated eye movement
  • Head turning in response to visual and auditory stimuli
115
Q

What is pupillary reflex?

A
  • Some optic nerve fibres are relayed to the parasympathetic nuclei, on both sides of the brain, of CNVIII, then to the ciliary ganglion.
  • Post ganglionic fibres cause pupillary constriction in both eyes.
116
Q

How are the 2nd and 3rd cranial nerves tested for?

A

Testing CNII and CNIII (PS component): shining a light into the animal’s eyes. When you shine a light in one eyes, both pupils should constrict due to the optic chiasm.

Sensory – CNII. Motor – CNIII.

117
Q

How can the 2nd and 7th cranial nerves be tested for?

A

Menacing gesture causes eyelid closure. Tests CNII and CNVII and requires:

  • Normal functioning eyes
  • An intact visual pathway and cortex
  • Intact facial nerve
118
Q

What can be caused by damage to the 3rd, 4th and 6th cranial nerves?

A
  • Normal position of the eye depends on the function of the cranial nerves III, IV and VI.
  • Damage to the nerves can cause eyeball to be abnormally positioned (strabismus = squint)
119
Q

How are the 3rd, 4th and 6th cranial nerves tested?

A
  • Assess cranial nerves related to eye movements by assessing vestibulo-ocular reflex.
  • Swiftly move the animal’s head in a horizontal/dorsal plane from side to side
  • Occurs even if blind/eyes closed/in dark
  • Eye movements have phases: slow phase and fast phase
120
Q

Describe the fibres in the brain.

A

Commissural fibres – between hemispheres, corpus callosum

Association fibres – joining bits of the same hemisphere

Projection fibres – connects hemisphere with lower CNS, ascending and descending, internal capsule

121
Q

What are the basic functions of the cerebellum, pons, thalamus, corpus callosum and frontal lobe?

A

Cerebellum = coordination of movement and muscle tone, balance and posture.

Pons = eye muscle coordination

Thalamus = major sensory relay

Corpus callosum = allows communication between the 2 hemispheres

Frontal lobe = conscious perception

122
Q

What is the covering* of the brain made out of?

A

Dura mater

123
Q

What is the fissure separating the 2 hemispheres called?

A

Longitudinal fissure

124
Q

What do the rostral cerebral arteries supply?

A

Medial surface of the cerebral hemisphere

125
Q

Describe the structure of CNV trigeminal nerve.

A
  • The largest cranial nerve
  • Attached to brainstem at junction of pons and trapezoid body
  • Motor and sensory roots travel in a common sheath
  • Trigeminal ganglion contains cell bodies of general somatic afferent fibres of the trigeminal nerve
126
Q

Describe the V1 ophthalmic branch of CNV. How is this branch tested?

A
  • Sensory to skin on dorsum of nose, orbit, cornea, some of nasal cavity and sinus
  • Orbital fissure
  • Test with corneal and palpebral reflexes
127
Q

Describe the V2 maxillary branch of CNV. How is this branch tested?

A
  • Sensory to skin of cheek, side of nose, palate, nasopharynx mucosa, teeth and gums of upper jaw
  • Round foramen
  • Test with palpebral and vibrissae reflexes
128
Q

Describe the V3 mandibular branch of CNV. How is this tested?

A
  • Mixed
  • Sensory to muscles of mastication, lower teeth and gums
  • Oval foramen
  • Look for muscle asymmetry
129
Q

Describe the palpebral reflex.

A
  • Tests ophthalmic and maxillary branches of CNV trigeminal nerve and CNVII
  • Touch each cantus to see if they blink – lateral canthus for maxillary and medial for ophthalmic
130
Q

Describe the corneal reflex.

A
  • Gently touch cornea and the animal blinks
  • Can also be used to monitor deep anaesthesia
  • Sensory of ophthalmic branch of CNV trigeminal nerve
  • Motor of CNVII
131
Q

How are CNV and CNVII assessed?

A

Palpebral reflex

Corneal reflex

Vibrissae response – twitching of the face when you touch the whiskers

Look for asymmetry
- Atrophy of muscles of mastication
- Weakened muscles of facial expression

132
Q

What are the CNVII and CNVIII cranial nerves and where do they emerge?

A

CNVII = facial
CNVIII = vestibulocochlear

Emerge superficially from the junction between the pons and medulla and are closely associated.

133
Q

Describe the structure and function of the vestibular apparatus.

A

Specialised receptors in the inner ear which detect rotational movements of the head and the position of the head with respect to gravity. A series of hair cells in the cochlear and semi-circle canals to cause the bones to vibrate and create sound waves for hearing and proprioception.

134
Q

Describe the vestibular nuclei connections.

A
  1. Receptors in semi-circular canals and macula that send information to the brain vua the vestibular ganglion
  2. At level of braincell and aggregates come together form vestibular nuclei, deep within the medulla
  3. Cerebellar input for feedback control of movement to vestibular nuclei
  4. Inputs to the thalamus and so cerebral cortex for conscious awareness of balance.
  5. Also goes to medial longitudinal fasciculus for control of extrinsic eye movements
  6. To vestibulospinal tract for reflex control of ipsilateral muscles
  7. Finally goes also to medullary reticular formation, control for vomiting centres and cardiovascular responses to motion
135
Q

What is vestibular disease?

A
  • Vestibular disease is common: vestibular apparatus or nerve and central
  • Head tilt/circling
  • Abnormal nystagmus
  • Vomiting
  • Incoordination
136
Q

Describe the cochlear component of CNVIII vestibulocochlear.

A
  • Cochlear transduces sound waves and is innervated by the cochlear nerve at cochlear nuclei
  • Lateral lemniscus
  • Caudal colliculus – facial nucleus controlling movement of the ears and reflex response via tectospinal tract
  • Thalamus via the medial geniculate nucleus
  • Internal capsule
  • Auditory cortex where hearing is perceived
137
Q

How are auditory pathways tested?

A

Defects in hearing, especially unilateral, are difficult to assess. Test by startle response, which is absent if bilaterally deaf, presuming the tegmentum is intact.

138
Q

What are CNIX and CNX cranial nerves and how are they tested?

A

CNIX = glossopharyngeal
CNX = vagus

Examined together via the gag reflex, aka via the pharyngeal reflex.

139
Q

Describe the structure of the vagus nerve.

A

Recurrent laryngeal branch of the vagus nerve, CNX (vagus has parasympathetic and motor fibres as it descends from the head. Motor fibres branch up and loop around the aorta and become recurrent laryngeal nerve, while parasympathetic becomes parasympathetic innervation to the abdomen).

140
Q

What is CNXI and how is it examined?

A

CXI accessory (spinal) nerve examined by assessing neck muscle symmetry – trapezius, sternomastoideus, cleidomastoideus, cleidocervicalis, omotransversarius.

141
Q

What is CNXII and how is it examined?

A

XII hypoglossal nerve examined by opening the mouth and noting the size, shape and symmetry of the tongue. Touch the tongue and note the response and movement.

142
Q

What are the major afferent pathways?

A

Conscious sensations
- Special senses: vision, olfaction, hearing, balance
- Touch pressure and proprioception – medial lemniscal tract

Pain
- Spinoreticular tract
- Spinothalamic tract

143
Q

Name the major somatic motor pathways.

A
  • Corticospinal (pyramidal)
  • Rubrospinal (extra-pyramidal)
  • Tectospinal (extra-pyramidal)
  • Vestibulospinal (extra-pyramidal)
  • Reticulospinal (extra-pyramidal)
144
Q

Describe conscious proprioception via the medial lemniscal pathway.

A
  1. Mechanorecptors > spinal cord in general somatic afferent neurones.
  2. Ascend in the dorsal column/funiculus – there are 2 main divisions: gracile (long) and cuneate (wedge shaped) fasciculi.
  3. Information to the brain via dorsal root ganglion.
  4. Gracile and cuneate nuclei on dorsal medulla oblongata, where they synapse (no longer ipsilateral)
  5. Axons decussate to lie contralaterally and run in the medial meniscus fibre tract.
  6. Neurones 3 in the thalamaus projects to the sensory cortex via the internal capsule.
145
Q

Describe the paw replacement reaction.

A

Detection and reaction. List animals leg up and lift paw under and place back down. See if animal corrects itself.

146
Q

Describe the hopping response.

A

Evaluate all components required for voluntary limb movement. Get animals paw off the ground to make it unstable and then push over to see if there is a natural hop over to the other side.

147
Q

Describe the wheelbarrowing test.

A

Wheelbarrowing in small animals of thoracic limb and pelvic limb. See if the animal corrects itself.

148
Q

Describe the reliability of these proprioceptive and postural tests.

A

Less reliable in cats than dogs, as they are able to keep in this position for longer.

149
Q

Name the funiculi that pain is found in.

A

Found in all funiculi: ventral or lateral funiculus.

  • Spinoreticular – VF. Spine to reticular formation
  • Spinothalamic – LF. Spine to thalamus
  • Spinomesencephalic – VF. Spine to midbrain
  • Spinaovicothalamic – LF. Spine to cervical region of the thalamus
150
Q

What is required for conscious perception?

A

All funiculi project to somatosensory cortex via thalamus. Multiple, bilaterally-represented pathways for conveying noxious stimuli to brain. In pain pathways, there is decussation to other side of the spinal cord.

151
Q

How is pain assessed?

A

By compressing skin at base of digit. Compress skin fold on body surface and lightly touch nasal mucosa.

152
Q

What do lesions affecting general somatic afferent function cause?

A
  • Partial or complete loss of reflexes/ hyporeflexia and areflexia
  • Loss of nociception – hypalgesia/analgesia
153
Q

What are the 2 divisions of descending motor tracts in somatic efferent systems?

A

Pyramidal/corticospinal - found in all species but more important to those with more complicated motor tracts.

Subcortical/extrapyramidal - multisynapatic, such as rubrospinal originating from the red nucleus, vestibulospinal originating from vestibular nuclei, tectospinal originates from tectum of midbrain for auditory and visual inputs to the spine, reticulospinal is less known.

154
Q

Describe upper motor neurones.

A
  • Completely contained within the CNS
  • In red nucleus as well
  • Initiate voluntary movement
  • Maintain muscle tone
  • Regulate posture
155
Q

Describe lower motor neurones.

A
  • General somatic efferent to skeletal muscle
  • Cell bodies in ventral horn of spinal cord or in cranial nerve nuclei
  • Axons project into the PNS via cranial or spinal nerves and connect with muscle at the neuromuscular junction
156
Q

Describe the pathway of upper motor neurones in the corticospinal tract.

A
  1. Internal capsule
  2. Crus cerebri
  3. Pyramids – some decussate to comes out lateral corticospinal tract and some remain ipsilateral – comes out ventral corticospinal tract.
  4. Synapse in ventral horn
  5. Final common pathway is a motor neurone – alpha and gamma.
157
Q

What is 2/3 of the neurone pathway?

A

There is a 2/3 neurone pathway from cerebrum to spinal cord via medullary pyramids.

158
Q

What is paresis?

A

Deficiency in gait generation or the ability to support weight.

Upper motor neurone = spastic. Overall weakness

Lower motor neurone = flaccid. Loss of tone

159
Q

What is paralysis/paraplegia and what is ataxia?

A

Paralysis/paraplegia – complete loss of muscle function.

Ataxia – incoordination. Stumbling movements

160
Q

What is upper motor neurone disease/spastic paresis/paralysis?

A
  • Deficiency in gait generation
  • Loss of inhibition of anti-gravity extensors
  • Can support weight
  • Reflexes are normal to increases
  • Atrophy is disuse to milk generalised
  • Tone is normal to increased
  • Tetany
161
Q

What is lower motor neurones disease/flaccid paresis/paralysis?

A
  • Loss of ability to support weight
  • Atrophy and so unable to weightbear
  • Reflexes are decreased to absent
  • Atrophy is neurogenic
  • Tone is decreased to absent
162
Q

What are 3 aims of neurological exams?

A

To determine:

  • Whether the problems is neurological or orthopaedic
  • Whether the problem is in the brain or spinal cord
  • At what level of spinal cord the lesion is located
163
Q

How is muscle assessed?

A
  • Flex and extend muscles
  • Palpate for atrophy
164
Q

How are reflexes assessed?

A
  • Patella reflex – can be absent in dogs aged over ten
  • Withdrawal flexor-reflex – pinch thoracic and pelvic limb. Noxious stimulus.
  • Perineal reflex – S1-3. Tension of sphincter or flexion of the tail
  • Cutaneous trunci reflex
165
Q

What structures do upper motor neurone brain diseases affect?

A
  • Midbrain – red nucleus and substantia nigra
  • Pons – reticulospinal tracts
  • Medulla – reticulospinal tracts
  • Cerebellum, causing ataxia
166
Q

Distinguish tetraparesis and tetraplegia with paraparesia and paraplegia.

A

Tetraparesis and tetraplegia affects all 4 limbs and paraparesis and paraplegia only affected the 2 hindlimbs.

167
Q

What does lesioning at C1-C5 result in?

A

Lesion at C1-C5 cuts off upper motor neurones to all the limbs.

168
Q

What does lesioning at C6-T2 result in?

A

Cuts of upper motor neurones to pelvic limbs and the lower motor neurones to the thoracic limbs.

169
Q

What does lesioning at T3 and lower result in?

A

Lesion at T3 or lower, all limbs/thoracic limbs not affected so no longer tetrapareis or tetraplegia, and is paraparesis and paraplegia.

170
Q

Describe the distribution of upper and lower motor neurones along the spinal cord.

A

Lower down lesions the pelvic limbs supplied by upper motor neurones.

Lower motor neurones lesioned at L4-S1 to pelvic limbs.

171
Q

What does lesioning at S1 and lower reuslt in?

A

Cut off lower motor neurones to general somatic afferents. Deficit: tail, anus perineum

172
Q

What does lesioning at C1-T2 result in?

A

C1-T2 lesioning leads to ataxia in all limbs and hypalgesia in all limbs

173
Q

What does lesioning at T3-S1 result in?

A

T3-S1 lesioning has ataxia at pelvic limbs and hypalgesia-analgesia pelvic limb/trunk caudal to lesion.

174
Q

List the functions of the basal nuclei in the telencephalon.

A
  • Control of voluntary movement
  • Procedural learning
  • Eye movement
  • Cognition
  • Emotion
175
Q

List the symptoms of the basal nuclei in the telencephalon.

A

Dyskinesia – shuffling/abnormal gait and unsteadiness on limbs

Increased muscle tone so rigidity

176
Q

List the functions of the thalamus in the diencephalon.

A
  • Relay to and from cerebral cortex
  • Processing of sensations – touch, pain and proprioception
  • Consciousness
177
Q

List the functions of the hypothalamus.

A
  • Autonomic control via connections with the reticular formations
  • Homeostasis
  • Sleep
  • Behaviour
  • Control of pituitary
178
Q

List the collective symptoms of the diencephalon.

A
  • Abnormal behaviours
  • Totally body hypalgesia
  • Slow postural reactions
  • Depression leading to coma (ARAS)
  • Blindness
  • Alterations in thermoregulation and th8rst, etc
179
Q

List the functions of the components of the midbrain.

A
  • Reticular formation – involved in ARAS (alertness levels etc)
  • Red nucleus, substantia nigra and crus cerebri – containing motor tracts
  • Tegmentum – containing sensory tracts
  • Control of extraocular muscles, ciliary body and iris via oculomotor nerve
180
Q

List the symptoms of the midbrain.

A
  • Depression > coma
  • Ataxia
  • Stiffness with reduced voluntary function of muscles (spastic tetraparesis)
  • Hypalgesia
  • Deviation of the eye – strabismus
  • Dilation of the pupil
181
Q

List the functions of the cerebellum.

A
  • Balance/posture
  • Fine motor control - modifies intended movement
  • Ipsilateral function – such as the left cerebellar hemisphere controls left side of body
182
Q

List the symptoms of the cerebellum.

A
  • Ataxia (all legs)
  • Wide based stance (to correct the ataxia)
  • Tremor
  • Loss of balance
  • Dysmetria – overstepping
183
Q

What are the structures implicated in mental status?

A

Cerebral cortex
Relay (thalamus)
ARAS
Sensory system

184
Q

List the symptoms of mental status.

A

Alert and responsive
Depressed
Lethargic
Obtunded
Stupor
Coma

185
Q

Describe the extra-ocular muscles.

A
  • 4 rectus muscles
  • Oblique muscles
  • Different combinations of contraction of these muscles allow movement of the eyeball
  • Retractor bulbi allows the eye to be retracted back into the orbit (protective mechanisms) and the abducent nerve supplies this.
186
Q

Name the cranial nerves related to eye movement and describe how to test these.

A
  • Assess cranial nerves related to eye movements by assessing vestibulo-ocular reflex.
  • Swiftly move the animal’s head in a horizontal/dorsal plane from side to side
  • Occurs even if blind/eyes closed/in dark
  • Eye movements have phases: slow phase to track things and fast phase to snap focus back to another target
187
Q

Describe the vestibulocular reflex.

A

Stabilise gaze during head movement by producing eye movements in the direction opposite to head movement.

  • Does not rely in visual input as sensory input is from the vestibular system.
  • Sensory arm CNVIII via the medial longitudinal pathway.
  • Motor arm CNIII, CNIV and CNVI to the extra-ocular muscles.
188
Q

How is the vestibulocular reflex tested?

A

Sensory: nystagmus, beats with fast phase of eye movement to follow eyes with lateral head movement. Strabismus and positional strabismus to see position and symmetry of eye to test CNIII.

Motor: CNIII by pupillary light reflex.

189
Q

What is vestibular syndrome?

A

Affects balance and coordination caused by any condition that affects the balance centres in the ear and brain.

190
Q

Describe the structure and function of the vestibular apparatus.

A

The vestibular apparatus is responsible for maintaining balance, posture and the body’s orientation in space. Also regulates locomotion and other movements and keep objects in visual focus as the body moves. Vestibular system is comprised of the semi-circular canals, the vsetibocochlear nerve CNVIII and the parts of the brain that interpret and respond to information derived from these structures.

191
Q

List the clinical signs of vestibular syndrome.

A
  • Falling
  • Head tilt
  • Nystagmus
  • General wobbliness
  • Circling
  • Vomiting/nausea – balance centre is very close to vomiting centre of the brain
  • Facial paralysis – balance centre is very close to the hearing sensors in the ear and the facial nerve CNVII
  • Hearing loss – balance sensors are found within the ear closely associated with the hearing centres
  • Diseases affecting the balance centre in the brain can also affect other parts of the brain, causing seizures, weakness, loss of vision or difficulty eating and drinking.
192
Q

What are the causes of vestibular syndrome?

A
  • Idiopathic – especially geriatric dogs for unknown reasons
  • Otits interna
  • Brain lesion
  • Toxins
193
Q

How can vestibular syndrome be diagnosed?

A
  • Otoscopic examination and a swab taken if an infection is suspected
  • May have no typical signs of ear inflammation such as head shaking, scratching of the ear, inflamed ear canal or inflamed eardrum
  • Diagnostic imaging – X-rays, CT and MRI
  • CSF tap
194
Q

How can vestibular syndrome be treated?

A

Treat underlying cause, for example, otitis.

Supportive care, such as anti-nausea meds and nursing care.

195
Q

What is the prognosis of vestibular syndrome?

A

Dependent on underlying cause. Idiopathic vestibular syndrome may recover typically in a few days.

196
Q

Outline the corticospinal tract.

A
  1. UMN originate in left primary motor cortex
  2. Pass through internal cortex
  3. Brainstem and crus cerebri
  4. Medulla pyramids in hindbrain where they decussate
  5. Synapse with LMN at anterior lobe of the spinal cord at correct level of the spinal cord
  6. LMN of specific skeletal muscles

Those that do not decussate and travel to the proximal muscles travel in the anterior corticospinal tract of the spinal tract and decussate at the level of the spinal cord with the LMN.

197
Q

Describe the rubrospinal tract.

A
  • Originates in red nucleus and is also under voluntary control
  • Decussate and descends in the lateral aspect of the spinal cord where it synapses with a LMN
  • Targets LMN that facilitate in muscle flexion and inhibits neurones in muscle extension
198
Q

What are the causes of upper and lower motor neurone lesions?

A
  • Any injury such as infection stroke or tumour UMN
  • Injury to the white matter of the spinal cord UMN
  • Injury o exons leaving spinal cord LMN
  • Injury to spinal cord itself and anterior lobe of spinal cord LMN
  • Also arises from MSK problems like necrotising myopathies, hyper/hypokalaemia, NMJ disorders (such as myasthenia gravis, botulism and aminoglycoside toxicity)
199
Q

What are the signs of UMN lesions?

A
  • Little/no muscle atrophy
  • Weakness
  • Hyper reflexive as there are no UMN that are regulating reflex at that level
  • Diminished/absent superficial reflex
200
Q

What are the signs of lower motor neurone lesion?

A
  • Atrophy
  • Flaccid paralysis
  • No plantar response
  • Absent tendon reflexes
  • Visible fasciculations
201
Q

What are the possible locations of spinal cord lesions?

A

Cervical C1-C5
Cervical intumescence C6-T2
Thoracolumbar T3-L3
Lumbosacral intumescence L4-S3
Caudal segments Cd1-Cd5

202
Q

Distinguish what happens when lesions of the spinal cord occur at and cranial to an intumescence.

A

At an intumescence, it can damage LMN cell bodies supplying the limbs, resulting in LMN signs such as reduced/lost reflexes, atrophy of specific muscles, reduced muscle tone.

Cranial to the intumescence, LMN intact for good tone and intact reflex arcs to those limbs, and animal has UMN signs, such as UMN compromise to limbs.

203
Q

What is Wobbler’s syndrome?

A

Wobbler’s syndrome = cervical vertebrae stenotic myelopathy

  • 2-3% prevalence in thoroughbreds.
  • Characterised by abnormal gait in the front and/or hind limbs with a varying degree of incoordination and weakness.
  • Onset of clinical signs 6 months – 3 years. Mature horses may also become affected.
204
Q

What are the 2 main anatomical features of Wobbler’s syndrome?

A

Narrowing of the cervical vertebrae canal through which runs the spinal cord

Dynamic compression of the spinal cord by the cervical vertebrae

205
Q

What are the clinical signs of Wobbler’s syndrome?

A
  • Sway/stumble in pelvic limbs with overreaching in thoracic limbs (floating)
  • Stiff limbs and slapping noises as hooves hit the floor
  • Stumbles when walking when head raised
  • Difficulty turning in tight circles
206
Q

What are the 2 possible treatments types for Wobbler’s syndrome?

A

Surgical – metal brackets to stabilise join and relieve compression only young mildly affected horses are good surgical candidates

Medical – anti-inflammatory treatment, steroid spinal injections, dietary management

207
Q

Outline the process of the ventricular system.

A
  • Lateral ventricles have caudal and rostral horns.
  • Lateral ventricles contain choroid plexus that makes CSF. Choroid plexus formed from epenchymal cells.
  • Septum pellucidum separates the lateral ventricles.
  • Lateral ventricles drain to the 3rd ventricle in the middle via a foramen.
  • 3rd ventricle has the cerebral aqueduct to the 4th ventricle.
  • 4th ventricle is in the rhombencephalon.
  • Drains from the 4th ventricle to the arachnoid space and so spinal cord via the 2 lateral apertures/foramen Lushka and the medial aperture/foramen Megendi.
208
Q

Describe each layer surrounding the brain.

A
  • Dura mater around the brain.
  • Layer of dura beneath dura mater.
  • No epidural space as periosteum adheres dura mater to the skull.
  • No subdural in the skull but in the spinal cord, there is subdural and no periosteum.
  • Arachnoid mater with trabeculae/granulations.
  • Subarachnoid space has CSF.
  • Pia mater is one cell thick.
  • Tegmentum is part of the dura mater separating the cerebellum and cerebrum.
  • Falx cerebri separates cerebral hemispheres and falx cerebelli separates the cerebellar hemispheres
  • Venous sinuses are gaps between Dural layers.
  • Cisterns are widened areas of subarachnoid space containing CSF.
209
Q

Which information is not conveyed by the brain?

A

Olfaction

210
Q

What tethers the spinal cord in place caudally?

A

Filum terminale

211
Q

For each cranial nerve, state whether it contains sensory, motor or both fibres.

A

Olfactory I = sensory
Optic II = sensory
Oculomotor III = motor
Trochlear IV = motor
Trigeminal V = motor and sensory
Abducent VI = motor
Facial VII = motor and sensory
Vestibulocochlear VIII = sensory
Glossopharyngeal IX = motor and sensory
Vagus X = motor and sensory
Accessory XI = motor
Hypoglossal XII = motor

212
Q

Which branch of which nerve carries sensory information for the corneal reflex?

A

V1 ophthalmic branch of trigeminal nerve V

213
Q

Which cranial nerve supplies the majority of the muscles of the eye?

A

Oculomotor III

214
Q

Which cranial nerves are sensory and motor to the menace response?

A

Optic II and facial VII

215
Q

In which lobe is olfactory information processed?

A

Piriform lobe

216
Q

Which cranial nerves are involved in the sensory and motor parts of the pupillary light reflex?

A

Sensory = optic II
Motor = oculomotor III

217
Q

Which nerves are tested by the corneal reflex?

A

V1 and VII

218
Q

Which artery provides the major supply to the cerebral arterial circle in the dog?

A

Internal carotid

219
Q

What space does the hippocampus lie in?

A

Lateral ventricle

220
Q

Which cranial nerves are tested by the vestibulo-ocular reflex?

A

Oculomotor III
Trochlear IV
Abducent VI
Vestibulocochlear VIII

221
Q

What is neurolocalisation?

A

The aim is to find 1 location that explain all the clinical signs found on the neurological exam. Only if 1 location cannot explain all the signs can you consider a multifocal localisation. Possible locations:

  • Forebrain
  • Brainstem
  • Vestibular/cerebellum
  • Spinal cord
  • Lower motor neurone, neuromuscular junction, muscle
  • Unilateral vs bilateral
222
Q

How can you neurolocalise a case?

A
  1. Are there any signs of central (brain) disease?
  2. Which legs are affected?
  3. Which sort of tests allows to check which legs are affected?
  4. Is it 1 sided or both sided?
  5. What do the local reflexes tell us?
223
Q

What are the typical clinical signs of a cervical or thoracic spinal cord lesion?

A
  • Pain
  • Nociceptive and/or motor deficits
  • No nystagmus
224
Q

What are the typical clinical signs of a forebrain lesion?

A
  • Abnormal consciousness
  • Seizures
  • Blindness
  • Circling
225
Q

What are the typical clinical signs of thalamus lesions?

A
  • Obtunding of senses
  • Abnormal behaviour
226
Q

What are the typical clinical signs of vestibular lesion?

A
  • Nystagmus
  • Head tilt
  • Proprioceptive deficits
227
Q

Based on the location to peripheral vestibular disease, the list of possible causes is listed using the mnemonic VITAMIND.

A

Vascular – not possible based on localisation

Infectious/inflammatory – possible with history of otitis externa

Trauma/toxic – possible. Some ear drops are ototoxic

Anomaly – not possible

Metabolic – unlikely. Hyperthyroidism is possible bit would expect other clinical signs.

Idiopathic – possible although usually in older dogs

Neoplastic – possible

Degenerative – not consistent with sudden onset