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Neuro Flashcards

1
Q

Describe the meningeal layers

A
  • From superficial to deep
  • Dura mater -> periosteal layer adheres to skull, meningeal layer adheres to periosteal layer except at dural venous sinuses
  • Arachnoid mater -> adhered loosely to dura mater. Has sub arachnoid space below
  • Pia mater -> closely adhered to gyri and sulci
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2
Q

Describe the ventricular system of the brain

A
  • Two lateral ventricles joined to third ventricle through ventricular foramen, joined to forth ventricle through cerebral aquaduct, all lined by ependymal cells
  • Houses choroid plexus which produces CSF
  • Drains from 4th ventricle into central canal and subarachnoid space -> arachnoid granulations into dural venous sinuses
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3
Q

List the major functions of the frontal lobe

A
  • Houses pre-central gyrus (primary motor cortex)
  • Brocas area for expressing speech
  • Behaviour and personality
  • Problem solving
  • thinking
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4
Q

List the major functions of the parietal lobe

A
  • Houses post-central gyrus (primary sensory cortex)
  • Spacial and body awareness
  • Language
  • Attention
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5
Q

List the major functions of the temporal lobe

A
  • Auditory cortex
  • Memory
  • Wernickes area for understanding and processing speech
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6
Q

List the major functions of the occipital lobe

A

-Visual cortex

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7
Q

List the major functions of the cerebellum

A
  • Planning and coordination

- Balance and proprioception

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8
Q

Briefly describe the different types of glial cells

A
  • Astrocytes -> star-shaped cells which support the bbb, provide nutrients and maintain ECF
  • Oligodendrocytes -> Myelinate multiple CNS axons
  • Ependymal cells -> Line the ventricular system and central canal -> circulate CSF
  • Microglia -> immune cells of cns (phagocytes)
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9
Q

Describe the diseases produced upon failure of closure of the neural tube

i) cranially
ii) caudally

A

i) ancephaly -> incompatible with life
ii) Spina Bifida -> most commonly lumbosacral. SB meningocoele is when there are when spinal tissue is covered in meninges. It produced mild symptoms. SB myelomeningocoele is when neurological tissue is exposed, produces severe symptoms. SB oculta is loss of spinous processes, often produces no symptoms
- Symptoms include hydrocephalus, poor ability to walk, incontinence

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10
Q

What is rachishisis?

A

-Failure of the neural tube fold to elevate out of the plane causing ancephaly

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11
Q

How are neural tube defects diagnosed? How can they be prevented?

A
  • Raised maternal serum a-fetoprotein
  • USS
  • Preconceptual and 1st trimester folic acid
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12
Q

Why does the corda equina develop?

A

-Vertebral column grows faster then SC meaning spinal roots must elongate to exit at the corresponding intervertebral foramen

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13
Q

After the 3 primordia of the brain develop, how do they progress and into what areas of the brain do they develop?

A
  • Prosencephalon -> telencephalon (cerebral hemispheres) and diencephalon (thalamas)
  • Mesencephalon -> midbrain
  • Rhombencephalon -> melencephalon (pons/cerebellum) and myelencephalon (medulla oblongata)
  • 2 flexures develop due to lack of space ->cervical between spinal cord and hind brain and cephalic between midbrain and cerebrum
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14
Q

Give a communicating and non-communicating cause of hydrocephalus

A
  • Non-communicating = cerebral aquaduct sternosis/arnold-chiari
  • Communicating = arachnoiditis/meningitis
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15
Q

Name 3 diseases involved in failure of neural crest cells

A
  • Digeorge (CATCH22)
  • CHARGE syndrome
  • Hirchsprungs (aganglionic megacolon)
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16
Q

Describe in detail how the astrocytes provide nutrients for neurones, remove neurotransmitters and maintain the ionic environment

A
  • Use a glucose-lactate shunt -> take up glucose and store it as glycogen. When brain needs it converts glycogen -> lactate by anaerobic respiration. Lactate can be used in brain in times of need
  • Use reuptake transporters to reuptake neurotransmitters such as glutamate into cells to keep EC concentrations low. Once uptaken glutamate recycled to glutamine
  • Maintain ionic environment as neuronal activity raises [k]ec which is taken up by astrocytes to prevent inappropriate electrical activity of neurones
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17
Q

What makes up the bbb? What is the function of the bbb?

A
  • Brain capillary endothelia joined by tight junctions, pericyte, foot processes of astrocytes
  • Limits diffusion of blood product into csf to support the environment for neurones
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18
Q

Describe the different types of neurotransmitters (class and excitatory or inhibitory)

A
  • Amino acid -> glutamate (excitatory), glycine (brainstem/SC) and GABA (inhibitory)
  • Biogenic amines -> ach (mainly excitatory), dopamine, NA, serotonin
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19
Q

What types of receptor does glutamate act on? Which receptor is responsible for fast depolarisations? Which receptor is blocked by Mg? What is the consequence of this? What cortical function are glutamate receptors involved in?

A
  • NMDA and AMPA
  • AMPA is fast depolarising
  • NMDA is blocked by Mg and therefore requires lots of stimulation in order to activate it
  • Learning and memory
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20
Q

What type of ion channels are linked to GABA and glycine receptors? What happens when these neurotransmitters bind?

A
  • Cl-
  • Opens Cl- channels and Cl- enters the cell leading to hyperpolarisation -> decreased AP firing thus post synaptic potential inhibited
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21
Q

Which receptors do barbituates/benzos bind to? How do they modify this receptor? What outcome do they produce via this mechanism? When are they used? What is the risk of using them?

A
  • GABAa receptors
  • Increase the receptors sensitivity to GABA
  • Anxiolytic and sedation via increasing inhibitory response of GABA binding
  • Anxiety, insomnia, status epilepticus
  • Dependance and fatal overdose
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22
Q

In which processes is Ach commonly found to be the neurotransmitter?

A
  • Parasympathetic
  • Motor
  • Arousal of CNS
  • Learning and memory
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23
Q

Why are AchE inhibitors sometimes used in Alzheimer’s?

A

-Degeneration of nucleus basalis which houses ach neurones. AchE inhibitors potentiate action of remaining Ach neurones

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24
Q

What 4 pathways is dopamine involved in? What are 2 common diseases which involve dopamine dysfunction, and in what way is dopamine altered?

A
  • Nigrostriatal (Motor control)
  • Mesocortical and mesolimbic (mood, arousal and emotion)
  • Tubero-hypophyseal
  • Parkinsons (decreased) and Schizophrenia (increased)
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25
Q

What is the function of NA as a transmitter within the CNS?

A

-Behaviour arousal and mood

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26
Q

What are the functions of serotonin within the CNS?

A

-Sleep and mood

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27
Q

What is the difference between somatic and visceral sensation?

A
  • Visceral pain/sensation is diffuse and hard to localise and only detects stretch, ischaemia, and inflammation
  • Somatic sensation/pain is sharp and easy to localise and detects all types of sensation including 2-point discrimination and temperature
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28
Q

What are modalities and qualities when referring to sensation? What determines the modality/quality?

A
  • Modality is the subtype of sensation eg temperature/pressure etc
  • Quality is a subtype within the modality eg hot/cold
  • Determined by the type of receptor activated and how it is activated
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29
Q

How do APs relate to the intensity of sensory stimuli?

A

-The more intense the sensory stimuli, the higher the frequency/duration of APs due to a greater change in mp

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30
Q

Where do the cell bodies of 1st order neurones of DCML lay? What is a generator potential?

A
  • Dorsal root ganglion in PNS

- The AP produced at the receptor by opening of Na channels in response to a sensory stimulus

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31
Q

What are meissners corpuscles/merkels discs?

A

-Cutaneous mechanoreceptor found in high density at the fingertips responsible for light touch and vibrations -> rapidly adapting

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32
Q

What are pacinian corpusles?

A

-Cutaneous mechanoreceptor responsible for vibration and pressure -> rapidly adapting

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33
Q

What are ruffini endings?

A

-Cutaneous mechanoreceptors which detect stretch and involved in proprioception -> very slow adapting

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34
Q

What are tonic receptors? What are phasic receptors?

A
  • Receptors which respond continuously to a stimulus ie they are slowly adapting
  • Receptors which rapidly adapt to a stimulus meaning they no longer respond
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35
Q

What is sensory acuity? What is lateral inhibition?

A
  • Refers to the size of a receptive field of a neurone. The smaller the receptive field the greater the acuity meaning that it is possible to locate a stimulus to a smaller area
  • Lateral inhibition is a process which enhances sensory acuity -> when a neurone is stimulated in a receptive field it inhibits neighbouring neurones through inhibitory interneurones enabling more localisation of the signal
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36
Q

What is somatotopy?

A

-The idea that every point on the body has a 1:1 correspondence in the CNS ie the sensory homunculus

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37
Q

What modalities are detected by the DCML? Describe the DCML pathway

A
  • Fine touch, vibration, 2-point discrimination and proprioception
  • Sensory afferent (1 neurone) detect stimulus and enters spinal cord and travels up to medulla and synapses on 2 neurone. 2 neurone decussates and travels to thalamus (internal arcuate fibres). 3 neurone projects to cortex
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38
Q

In regards to DCML, where is the 1 neurone cell body? When synapsing in the medulla, where specifically do neurones synapse? Describe the organisation of fibres in the DCML

A
  • Dorsal root ganglion
  • Neurones of C1-T5 synapse in the cuneate nucleus
  • Neurones T6-S5 synapse in the gracile nucleus
  • The lower body fibres are the most medial ie sacral then lumbar then thoracic the cervical
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39
Q

In regards to the DCML, if a lesion is below the medulla, what till the presenting sign be? Above the medulla? why?

A
  • Ipsilateral sensory loss
  • Contralateral sensory loss
  • Fibres decussate in the medulla meaning that before this point the information is regarding the ipsilateral side
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40
Q

What modalities are detected by the spinothalamic pathway? Describe the ST pathway

A
  • Crude touch, pain, temperature
  • Sensory afferents are stimulated and enter the spinal cord where they synapse immediately in the substantia gelatinosa or nucleus proprius (Rexed lamina 2,3 and 4). 2 neurone immediately decussates and ascends the spinal cord to the thalamus. 3rd order neurones from the thalamus to the cortex.
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41
Q

In regards to ST, where is the 1 neurone cell body? Describe the organisation of fibres in the ST

A
  • Dorsal Root ganglion

- They are organised with the upper limb running most medially ie cervical, thoracic, lumbar, sacral

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42
Q

In regards to the ST, if a lesion is within the CNS, what till the presenting sign be? In the PNS? why?

A
  • CNS will loose sensation to the contralateral side
  • PNS will loose sensation to the ipsilateral side
  • The 1st order neurone decussates immediately meaning that the information travelling in the spinal cord is from the contralateral side
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43
Q

What modalities are detected by the anterior spinocerebellar pathway? Describe the anterior spinocerebellar pathway

A
  • Unconcious proprioception of trunk and lower limb
  • Consists of 2 neurones -> 1 order neurone synapse immediately in dorsal horn -> travels up the spinal cord through superior cerebellar peduncle -> 2nd decussation -> cerebellar
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44
Q

If there is a lesion to the anterior spinocerebellar tract in the spinal cord what is the lesion? Lesion in cerebellum?

A
  • Loss on contralateral side

- Loss on ipsilateral side

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45
Q

What modalities are detected by the posterior spinocerebellar pathway? Describe the posterior spinocerebellar pathway

A
  • Unconscious proprioception of trunk and lower limb
  • No decussation -> 1st order neurones decussate in clarks column (nuckeus dorsalis) on ipsilateral side then travel up spinal cord to cerebellum through inferior cerebellar peduncle
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46
Q

What modalities are detected by the cuneocerebellar pathway? Describe the cuneoocerebellar pathway

A
  • Unconscious proprioception of upper limb and trunk

- Equivalent of posterior spinocerebellar but synapses in cuneate nucleus

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47
Q

What fibres are activated in response to pain? Describe the types of fibres, the NT used and the route to the cortex

A
  • Nociceptive fibres
  • Ad fibres -> Rapidly conducting producing intense, brief, well localised pain which result in a withdrawal reflex. Mainly associated with mechanoreceptors
  • C fibres -> slow conducting fibres which cause a dull, diffuse, long lasting pain. Associated with polymodal receptors
  • Glutamate and Substance P
  • Pain fibres -> dorsal horn -> synapse -> decussate -> join spinothalamic tract -> thalamas -> cortex. Some fibres peel off to reticular formation and others to periaquaductal grey matter
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48
Q

How do pain fibres from the head travel to cortex?

A
  • Anterior -> trigeminothalamic system

- Posterior -> Cranial nerves

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49
Q

What is thalamic pain? What type of drug does it respond to?

A
  • Pain neurones integrate with cutaneous neurones in the thalamus thus a thalamic lesion causes painful somatic sensations
  • Antiepiletics and amitriptyline (antdepressant)
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50
Q

What is phantom limb pain?

A

-A central pain caused by retained sensation of a limb after amputation.

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51
Q

What is chronic pain?

A

-Pain which has been occurring intermittently/constantly >3/12

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52
Q

What is mechanism of referred pain?

A

-Activation of visceral nociceptors producing pain at the body surface due to nocicepter fibres from viscera and sensory cutaneous fibres converging on a common dorsal horn. CNS cannot determine whether the source is superficial or deep and as sensory cutaneous fibres more active the pain is perceived as coming from there

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53
Q

What is the gate control theory of pain?

A
  • A theory that states that the activation of cutaneous mechanorecpetors inhibits nociceptive firing of the ST pathway
  • This is because usually cutaneous stimulation activates the nociceptive ST pathway as well as enkehpalinergic inhibitory interneurones in the substantia gelatinosa thus normal cutaneous stimuli is not painful as the nociceptive signal is not sent to the brain. This is peripheral regulation of pain
  • Noxious firing is based on the relative amount and intensity of nociceptive firing vs mechanofiring
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54
Q

Describe how pain is centrally regulated

A
  • The PAG has neurones which project onto the raphe nuclei of reticular formation as well as the dorsal horns of the spinal cord
  • These projections are inhibitory of nociceptive fibres (descending inhibition)
  • The RF releases serotonin and NA and modulates pain by causing activation of the inhibitory interneurones of the substantia gelatinosa
  • Also NA release from Locus ceruleus onto dorsal horn causes activation of inhibitory interneurones
  • Activation of PAG can be due to stress, strong emotion etc
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55
Q

What is hyperalgesia/allydonia?

A
  • Hyperalgesia= increased sensitivity to pain
  • Allydonia = normally innocuous stimuli perceived as painful due to tissue damage causing the release of bradykinin, histamine and PGs
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56
Q

What are reflex responses? Describe the stretch reflex

A
  • Stereotyped involuntary responses that operate on a reflex arc
    1) muscle spindle detects stretch and lengthens
    2) sensory afferent fires to dorsal horn -> synapse -> motor efferent leaves ventral horn to muscle target
    3) Effector organ contracts and antagonist muscle relaxes through inhibitory reflexes
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57
Q

What are rhythmic motor patterns?

A

-Sequences of stereotyped repetitive responses which are largely autonomic but may require some input to stop/start eg walking

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58
Q

What are the two fibres in the corticospinal tract and where do they run from/to? Where is the cell body of the LMN?

A
  • Upper motor neurone originates in primary motor cortex of frontal lobe(30%), Premotor (30%) and somatosensory (40%) and projects through posterior internal capsule to medulla where most decussate and form medullary pyramids then run down to spinal level where they synapse onto lower motor neurone which projects onto target muscle
  • Ventral horn of nuclei or brainstem
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59
Q

What are a and g motor neurones?

A
  • Types of LMN
  • a-LMN are large in diameter and myelinated. Project onto extrafusial skeletal muscle
  • g-LMN are small diameter and cause contraction of muscle spindle to alter tone and tension in response to sensory feedback
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60
Q

What is a motor unit? How does this define the type of movement produced?

A
  • A LMN and all the muscle fibres it innervates
  • Innervates lots of muscle fibres = strong movement
  • Innervates few muscle fibres = fine movements
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61
Q

What are golgi tendon organs?

A
  • Structures which detect contractile tension as they are located between muscle and tendon
  • As GTO is stretched it increases its firing rate and causes inhibition of the aLMN causing relaxation of the muscle
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62
Q

How is posture maintained?

A

-Stretch reflex is used to control movements at joints by detecting feedback from muscle spindles and determining the amount of tonic contraction agonist and antagonist muscles need.

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63
Q

What is the protective flexor reflex?

A
  • An inbuilt reflex to protect limbs from potentially noxious stimuli
  • Upon noxious stimulation flexors of effected limb contract and extensors relax allowing limb withdrawal
  • Concurrently contralateral extensors contract and flexors relax to aid postural support
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64
Q

Describe the different types of motor unit. In what order are the units recruited, and what controls the force of muscle?

A
  • S -> slow contracting, fatigue resistant, small force eg postural muscles
  • FR -> Fast conducting, fatigue resistant, low force eg walking
  • FF-> Fast conducting, fast fatigue, high force eg running
  • S->FF
  • Number, frequency and type of activation
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65
Q

How does the anterior corticospinal tract differ from lateral?

A

-Remains ipsilateral and supplies axial muscles and C1-T1

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66
Q

Why is the internal capsule at risk of stroke?

A

-Supplied by middle cerebral artery which is a common site of haemorrhagic stroke

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67
Q

Describe the corticobulbar tract

A
  • Controls muscles of facial expression and extraocular muscles
  • UMN project from cortex to synpase on cranial nerve nuclei -> LMN/CNs project to target muscles
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68
Q

What is the medial longitudinal fasiculus?

A

-Projections which run between the L+R extraocular nuclei which is essential for connecting left and right eye movements

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69
Q

Which cranial nerve nuclei receive bilateral innervation?

A

-Trigeminal, facial and nucleus ambiguus (CNs of pharynx and larynx)

70
Q

Describe the differences between an UMN and LMN lesion

A
  • Both have decreased power
  • LMN has wasting (Late sign in UMN)
  • Hypertonia in upper, hypotonia in lower
  • Hyperreflexia in upper, hyporeflexia in lower
  • Fasiculations in lower
  • Clonus, clasp knife and babinski in upper
71
Q

Why would someone who had had a stroe present with a flexed upper limb and extended lower limb?

A
  • UMN lesion so produces hypertonia

- Flexers are stronger than extensors in UL and Extensors stronger than flexors in LL

72
Q

Give 3 reasons of a UMN lesion

A
  • Stroke
  • MS
  • SOL
  • Cerebral palsy
  • Traumatic brain injury
73
Q

Give 3 reasons of a LMN lesion

A
  • Trauma
  • Myasthenia gravis
  • Motor neurone disease (ALS)
74
Q

Name the 4 extrapyramidal tracts. State their main function and whether they’re ipsilateral or contralateral

A
  • Vestibulospinal -> ipsilateral -> balance during movements
  • Reticulospinal -> ipsilateral -> posture and reflexes
  • Tectospinal -> contralateral -> eye-head movement to visual/auditory stimuli
  • Rubrospinal -> contralateral -> Tone of face/flexors of UL
75
Q

Describe the locations of the major descending tracts in the spinal cord

A
  • Lateral corticospinal = posteriolateral (large)

- Anterior corticospinal = anterior medial (small)

76
Q

Describe the locations of the major ascending tracts in the spinal cord

A
  • DCML = posteiomedial
  • Spinocerbellar = anterior and posterior most lateral
  • spinothalamic = anterior
77
Q

If there was a lesion to the corticospinal tract in the CNS what lesion would be produced? Where would the presentation be if the lesion was in the brain? Spinal cord?

A
  • UMN
  • Contralateral
  • Ipsilateral
78
Q

Which cranial nuclei are susceptible to paralysis with unilateral lesions? why? How do they present?

A
  • Hypoglossal -> deviation of the tongue towards the lesion due to the tongue being stronger on the opposite side causing it to pull that way
  • Anterior facial -> Spastic paralysis of lower half of affected face only as anterior facial nucleus is unilateral but posterior which supplies to upper half is bilateral
  • Spinal accessory -> unable to turn head towards lesion
79
Q

What is lichthiems disease?

A

-Degeneration of the spinal cord due to b12 deficiency

80
Q

What is tabes dorsalis?

A

-Degeneration of the dorsal column caused by neurosyphilis

81
Q

If there is a lesion to the ST within the CNS, where is the presentation?

A

-Contralateral side

82
Q

What is syringomyelia? Causes? How does it present?

A
  • Cyst formation within the surrounding white matter of the central canal which compresses the surrounding tissue, often in cervical distribution
  • Caused by arnold chiari malformation, tumour, scoliosis
  • Disrupts ST pathway causing pain and altered temp sensation in a cape like distribution. Can also causes weakness and numbness
83
Q

What is brown sequards? Give some causes

A
  • A term used to describe hemisection of the cord, often due to trauma (disc hernation, tumour)
  • Pt presents with hemiparesis on ipsilateral side, loss of fine touch, vibration, proprioception and 2 point discrimination on same side and loss of crude touch, pain and temp on on contralateral side
84
Q

Describe the 3 error correction loops in motor planning

A

1) Muscle -> SC -> muscle (fastest)
2) Muscle -> brainstem -> cerebellum-> brainstem-> muscle
3) Muscle -> brainstem -> thalamus -> cortex -> decision making -> brainstem -> muscle ie conscious error correction (slowest)

85
Q

How do the basal ganglia and cerebellum plan movement?

A
  • Cerebellum plans route of movement
  • Basal ganglia are responsible for size and speed of a movement
  • They are active before movement has been initiated
86
Q

Name and describe the different portions of the cerebellum and their respective function

A
  • Cerebrocerebellum -> lateral hemispheres of cerebellum. Involved in planning movements and motor learning as well as maintaining postural tone.
  • Vestibulocerebellum -> functional equivalent of flocculonodular lobe -> connected to cerebrocerebellum near cerebellar peduncles. Involved in balance and ocular reflexes
  • Spinocerebellum -> Functional equivalent of vermis -> superior portion of cerebellum -> Involved in error correction and gait
87
Q

Explain how the cerebellum controls error correction

A
  • Spinocerebellum has 2 maps for body. 1 for motor output and another for snesory feedback
  • Comparison of predicted vs actual using these maps allows for error correction
  • Correction is calculated using limb position, speed of movement and sensory feedback to make correction for 100ms in future so correction is not behind as sensory feedback has a loop time of 100ms
88
Q

Describe the presentation of a cerebellar lesion

A
  • Lesion will be on ipsilateral side
  • Dysdiadochokinesia -> Loss of motor planning and sequence causes inability to make rapid alternating movements
  • Dysmetria -> Loss of coordination and correction
  • Dysarthria -> monotonic speech which is fragmented and may be slurred
  • Ataxia -> wide based unstable gait with poor balance and coordination
  • Nystagmus
  • Intention tremor
  • Hypotonia
  • Inability to learn new movements -> cortical control will be required to perform new movements they will never become automated
89
Q

Give 3 possible causes of a cerebellar lesion

A
  • Posterior circulation stroke
  • Alcohol
  • Multiple Sclerosis
  • Trauma
  • Inherited -> friedreichs ataxia (autosomal recessive causing progressive damage to spinocerebellar tracts)
  • Epilepsy medication
  • SOL
90
Q

Name the nuclei which make up the basal ganglia

A
  • Caudate nucleus + Putamen = striatum
  • Globus pallidus externa + interna
  • Substantia nigra (pars compacta + reticulata)
  • Subthalamic nucleus
91
Q

What is the function of the direct/indirect pathway of the basal ganglia? How does dopamine alter this? Which receptor does it act on in each pathway? Where are the dopaminergic neurones from/to?

A
  • Facilitate movement via exciting the cortex
  • Inhibit movement by inhibiting inputs to the cortex
  • Stimulates the direct pathway to facilitate movement and inhibits the indirect pathway to facilitate movement
  • Direct = D1, indirect = D2
  • Substantia nigra (pars compacta) onto striatum
92
Q

Describe the pathophysiology of Parkinson’s and the 4 cardinal signs. When does it typically present?

A
  • Degeneration of dopaminergic neurones in the substantia nigra which decreases facilitation of movement generated by the basal ganglia
  • Tremor, rigidity (lead pipe or cogwheel), bradykinesia, loss of postural instability (late stage)
  • 60s onwards
93
Q

Why are levodopa and caridopa used in parkinsons? What are its ADRs. Why is it important to tell the patient not to take vitamin B6?

A
  • Levodopa is a dopamine precursor which replaces the lost dopamine (still need to have some neurone present). it crosses BBB but most is deactivated in gut wall.
  • Carbidopa is a dopa decarboxylase inhibitor which prevents dopamine being broken down in the peripheries allowing more to enter bbb
  • ADRs = NV, hypotension, dystonia, psychosis
  • Increases peripheral breakdown of LDOPA
94
Q

What is epilepsy? What is the physiological cause of epilepsy

A
  • Episodic discharge of abnormal high frequency electrical activity in the brain leading to seizures
  • Increased excitatory neuronal activity at generator site. Decreased inhibitory activity (decreased GABA). Loss of homeostatic control of neuronal activity
95
Q

Describe the presentations of partial seizures depending on generator site

A
  • Frontal seizure = involuntary motor disturbance and behavioural change
  • Temporal = abnormal sensations, hallucinations, deja/jamais vu
  • Parietal = clonus, numbness/tingling, rapid HR
  • Occipital = visual disturbances, hallucinations
96
Q

What is a generalised seizure?

A
  • A seizure which begins focally but spread across both hemispheres with a loss of consciousness
  • Can be tonic-clonic or absent
97
Q

What is status epilepticus?

A
  • Prolonged seizure for 30 mins or more or multiple siezures without recovery of consciousness in between.
  • Medical emergency which can cause SUDEP
98
Q

Give some precipitants of an epileptic seizure

A
  • Lights
  • Infection/general health
  • Brain disease/trauma
  • Metabolic disturbances
99
Q

With regards to the eye, What fibres make up the optic nerve? which fibres are responsible for which field of vision? Which fibres cross at the optic chiasm? Where does the optic tract begin and which fibres does it have?

A
  • Nasal and temporal
  • Nasal fibres detect temporal vision and temporal fibres detect nasal vision
  • Nasal fibres
  • After the optic chiasm, temporal fibres of ipsilataral side and nasal fibres of contralateral side
100
Q

Which nuclei does the optic tract synapse upon?

A

-Lateral geniculate

101
Q

If there was a total lesion to the optic nerve, what would be the presentation? Give an example of a lesion here

A
  • Ipsilateral monocular blindless and loss of consensual reflex
  • Multiple sclerosis
102
Q

If there was a lesion at the optic chiasm, what would be the presentation and why? What could this lesion be?

A
  • Bilateral temporal hemianopia
  • Would affect the nasal fibres of each eye causing a loss of the temporal fields
  • Pituitary macroadenoma
103
Q

If there was a lesion to the optic tract, what would be the presentation? Explain this presentation. Give a common cause

A
  • Contralateral homonymous hemianopia meaning that the vision is lost in the left or right field of each eye
  • The optic tract has the ipsilateral temporal so the ipsilateral eye would loose its nasal (right) field, and the contralateral nasal fibres so the contralateral eye would loose its temporal (right) field
  • Stroke
104
Q

What is macular sparing? What causes it?

A
  • Preservation of the macular function in an otherwise blind hemifield
  • The occipital lobe has a dual blood supply-> majority from PCA but the occipital pole of lobe from of MCA. if there is a POCS affecting PCA the macular will be spared as it is topographically represented by the occipital pole
105
Q

What is the cause of a contralateral homonymous superior/inferior quadrantanopia?

A
  • Damage to the optic radiation either in the parietal lobe causing loss of superior fibres producing inferior quadrantanopia or temporal lobe causing loss of inferior fibres producing superior quadrantanopia
  • Both can be caused by damage to occipital lobe
106
Q

Explain the pupillary light reflex

A
  • Light stimulates CNII which has sensory afferents to lateral geniculate nucleus and the pretectal area
  • Efferents from LGN project to visual cortex whilst an interneurone from the pretectal area stimulates L and R CNIII in the edinger westphal nuclei which causes constriction of both eyes using the pupillary constrictor
107
Q

What 3 movements are involves in the accomodation reflex and which muscles are responsible?

A
  • Covergence (m.rectus)
  • Constriction (Pupillae constrictor)
  • Convexity (Ciliary body)
108
Q

What is tonotopy?

A

-Describes the spatial arrangement of where different frequency of sounds causes resonation of the basilar membrane to resonate and thus transmit different sounds to the brain

109
Q

Describe the structures inside the cochlear and how this leads to hearing

A
  • Scala vestibuli and scala tympani are fluid filled cavities which sit either side of the scala media
  • Scala media contains the organ of corti which is responsible for transmitting sound to the cochlear nerve
  • The organ of corti is lined with hair cells which are responsible for sensing and amplifying sound by using stereocilia to detect vibrations
  • Bending of the stereocilia opens K channels generating a receptor potential which opens VOCC. Influx of Ca causes release of NTs which triggers an AP to the auditory cortex
110
Q

Which hair cells in the organ of corti sense sound and which amplify sound?

A
  • Inner hair cells sense sound

- Outer hair cells amplify sound

111
Q

How do outer hair cells amplify sound?

A

-Receptor potential caused by K influx causes elongation or contraction of OHC which vibrates the tectorial membrane which is detected by the IHCs

112
Q

How does sound travel from external to inner ear?

A

-Enters the external auditory meatus and vibrates the tympanic membrane which causes vibtration of stapes, malleous and incus -> vibrations pass into scala vestibuli and scala tympani depending on frequency which vibrates the basilar and Reissner membrane respectively which vibrates the organ of corti

113
Q

What two factors help localisation of sound?

A

-Timing and intensity of sound from both ears

114
Q

Describe the path of the cochlear nerve to auditory cortex

A

-Cochlear -> CNVIII -> cochlear nucleus and superior olivary nucleus in pons -> medial geniculate nucleus -> auditory cortex

115
Q

What are pyramidal cells?

A

-Cell bodies of the cerebral cortex

116
Q

What is cerebral dominance?

A

-Refers to how some neural functions are more dominant in one hemisphere than the other eg Brocas and Wernickes dysphasia are usually LHS dominant vs spatial and body awareness which is RHS dominant

117
Q

How are brocas and wernickes areas connected?

A

-arcuate fasicuclus

118
Q

Describe the pathway for repeating a heard word, speaking a written word and speaking a thought

A
  • Auditory cortex -> Wernickes -> Brocas -> cerebrum
  • Visual cortex -> Wernickes -> brocas -> cerebrum
  • Cerebrum -> wernickes -> brocas -> cerebrum
119
Q

What is declarative memory? What lobe is it associated with? What structure in the brain is cruicial for consolidating declarative memories?

A
  • Long term memory
  • Temporal
  • Hippocampus
120
Q

What is non-declarative memory?

A

-Memory associated with motor skills and emotion

121
Q

Why is memory describe as neuroplastic?

A

-You can train memory causing an increase in post-synaptic receptors and NT release

122
Q

Describe the aetiology of Alzheimers

A

-Abnormal protein deposition resulting in amyloid plaques and neurofibrillary tau tangles associated with cortical atrophy and decreased NT levels

123
Q

What investigations would you preform in Alzheimers?

A
  • Confusion screen -> FBCs, U and Es, LFTs, CRP, glucose, calcium, B12/folate, urine dip, mmse
  • MRI head
  • MSE
124
Q

How is alzheimers pharmacologically treated?

A
  • Anxiolytics
  • Antidepressants
  • Ace Inhibitors
125
Q

What is Creutzfeld-jakob disease?

A
  • A Prion disease which when ingested alters protons into prions
  • Associated with BSE
  • Also termed HIV dementia
126
Q

What are the 3 route of entry of infection into the brain?

A
  • Direct spread eg middle ear, face, skull fracture
  • Blood borne eg sepsis, infective endocarditis
  • Iatrogenic -> VP shunts, LP
127
Q

What is dementia?

A

-An acquired global impairment of intellect, reason and personality without an impairment of consciousness

128
Q

What is a meningioma?

A

-Benign tumour of the brain which is well localised in symptoms and slow growing

129
Q

What is an astrocytoma?

A

-An aggressive malignant tumour of astrocytes which spreads along nerve tracts and often presents with spinal secondaries

130
Q

What is arousal in terms of neurology?

A

-The emotional state associated with a goal or avoidinace of something noxious

131
Q

What is the reticular formation? What are the inputs/outputs to the reticular formation?

A
  • A structure which runs the length of the brainstem and is associated with consciousness as well as autonomic functions such as CVS, Resp and micturition
  • Inputs from Sensory system and cerebral cortex
  • Outputs to thalamus, hypothalamus and basal forebrain nuclei which change the activity of the cortex
132
Q

What NTs are involved in the outputs of the RF?

A
  • RF ->Thalamus (Ach)->Cortex (Glutamate)
  • RF-> Hypothalamus (Ach)-> Cortex (Histamine)
  • RF -> BFN (Ach -> Cortex (Ach)
133
Q

Describe the positive feedback loop which is established between RF and Cortex to control consciousness

A

-Cortex inputs to the RF which ultimately inputs to the cortex which stimulates input to the RF and so on

134
Q

What is consciousness?

A

-Involves awareness of both internal and external states

135
Q

What does the B wave represent on an EEG and at what frequency is it?

A
  • Awakeness

- 50Hz

136
Q

What does the a wave represent on an EEG and at what frequency is it?

A
  • Removal of visual input as wave becomes synchronised

- 10Hz

137
Q

What does the theta wave represent on an EEG and at what frequency is it?

A
  • Stage 1 of sleep and are interspersed between a waves showing a slowing of neuronal activity
  • 5Hz
138
Q

What does the sleep spindle and K complex represent on an EEG?

A
  • Stages 2 and 3 of sleep respectively on a background of theta waves
  • Sleep spindles are from a burst of activity within the thalamus as it resists sleep and K complexes are the intrinsic rate of the cortex
139
Q

What does the delta wave represent on an EEG and at what frequency is it?

A
  • Stage 4 of sleep showing the intrinsic rate of the cortex devoid of input
  • 1Hz
140
Q

What is REM sleep? What does it look like on an EEG?

A
  • Rapid eye movement sleep during which the person will be very difficult to rouse due to strong inhibition of the thalamus. Muscle tone is lost due to increased descending inhibition of LMNs whilst eye movements and trigeminal functions are preserved (nocturnal bruxism). There is also autonomic effects being pemile erection and loss of thermoregulation
  • Mimics b waves
141
Q

What is braindeath?

A

-Widespread cortical and brainstem damage producing a flat EEG

142
Q

What is a coma?

A

-Widespread cortical and brainstem damahe with various disordered EEG patterns and an unarousable and unresponsive patient. No sleep wake cycle

143
Q

What is permanent vegetative state?

A

-Widespread cortical damage with spontaneous eye opening. Can localise stimuli to brainstem and sleep wake cycles are detected

144
Q

What is locked in syndrome and what is its cause?

A
  • Loss of all somatic function from the pons down -> retains eye movement
  • Basilar artery stroke
145
Q

Briefly describe the mechanism of sleep

A
  • Sleep requires closing down the +ve feedback loop between the RF and the cortex
  • Inputs to the reticular formation are sensory, cerebral and visual.
    1) closing eyes removes input from the visual system to the RF. Removing a stimulus from the RF decreases the +ve feedback loop
    2) Laying still removes sensory input to the RF -> decreased output to the cortex -> decreased +ve feedback
    3) Quieting the mind reduces cortical input to RF and again inhibits the +ve feedback loop
    4) As the RF receives less input it decreases its output to the thalamus, and removes inhibition from inhibitory iterneurones which decreases input to the cortex -> decreased inputs to RF
146
Q

What is the purpose of sleep?

A
  • Enigmatic
  • Energy conservation and bodily repair
  • Memory consilidation
  • Clearance of extracellular debris
147
Q

What is insomnia?

A

-The inability to sleep, normally due a psychiatric illness eg anxiety causing an overactive cortex -> increased input to RF

148
Q

What is Narcolepsy?

A

-Spontaneous falling to sleep partially due to loss of orexic neurones from visual system to RF -> intermitently loosing input to RF

149
Q

What is delerium?

A

-An acute confusional state with fluctuating levels of arousal (hyper-hypo)and impaired awareness causing disorientation and hallucinations

150
Q

Describe the glasgow coma scale

A
  • A measure of consciousness based on eye opening, and verbal and motor abilities
  • Eye -> 1=none, 2=to pain 3=to verbal cues 4=spontaneous
  • Verbal-> 1=none 2=incomprehensible sounds 3=inappropriate 4=Confused 5=Orientated
  • Motor-> 1=none 2=decerebrate 3=decorticate 4=withdraws from pain 5=localises to the pain 6=obeys commands
151
Q

Describe decerebrate and decorticate postures

A
  • Decerebrate is an abnormal extensor response where there is adduction and extension of the UL, wrist pronated and fingers flexed. LL stiffly extended and plantar flexed. Lesion is below the red nucleus
  • Decorticate is an anbormal flexor response where by UL is adducted and elbow, wrists and fingers flexed, legs stiffly extended, internally rotated and plantarflexed -> corticospinal damage
152
Q

What is the oculocephalic reflex? Vestibulo-ocular reflex?

A
  • Holding eyes open rotate head side to side and up and down, eyes should move in opposite direction to head (dolls eyes)
  • Eyes move towards cold water but away from warm water in the ears
153
Q

Which vessels make up the anterior/posterior circulation?

A
  • Ant = ICA -> opthalmic, MCA (main branch), ACA and posterior communicating
  • Post = Vertebral -> Basilar, Posterior Cerebral, superior cerebrellar, anterior inferior cerebellar, posterior inferior cerebellar and pontine
154
Q

Which part of the brain does MCA supply? What are the symptoms of a MCA stroke (TACS)?

A
  • Lateral aspect of frontal, parietal and occipital
  • Contrlateral hemiparesis and hemisensory loss of face arm and leg
  • Contralateral homonymous hemianopia
  • Higher cortical dysfunction eg aphasia
  • Possible perceptual defects eg hemineglect
155
Q

Which part of the brain does the ACA supply? What would a stroke here present like (PACS)?

A
  • Medial frontal and parietal
  • 2/3 of:
  • Contrlateral hemiparesis and hemisensory loss of face arm and leg
  • Contralateral homonymous hemianopia
  • Higher cortical dysfunction eg aphasia
156
Q

What does the PCA supply? What will a stroke present like?

A
  • Thalamus, midbrain, temporal and occipital lobes
  • Depends on site of occlusion -> peripheral occlusion can include contralateral homonymous hemianopia, cortical blindness or agnosia. Central can cause contralateral hemiparesis, dystonia and thalamic pain
157
Q

What is a lacuna stroke?

A

-Stroke in one of the perforating arteries which supply the basal ganglia and pons

158
Q

Describe some causes of ischaemic stroke vs haemorrhages

A
  • Ischaemic = Large vessel atheroma/embolism, Cardiac embolism, Blood coagulopathy, Vasculitis
  • Haemorrhagic = Hypertensive microaneurysms, AV malformaton, thrombocytopenia, cocaine
159
Q

Describe the blood supply to the spinal cord and the region/tract it supplies

A
  • Anterior spinal from vertebral arteries is a single artery which supples 2oclock -> 10oclock (corticospinal, ST and spinocerebellar)
  • Posterior are paired arteries supply between 10-2 (DCML)
160
Q

Where is an extradural haematoma? What does it look like on CT? What causes it? How does it present?

A
  • Between dura mater and skull caused by an arterial bleed
  • Looks like Egg on CT, maybe midline shift and loss of ventricle, can be limited by sutures
  • Normally caused by head trauma
  • Immediate lucid period then recovery. Delay before symptoms become evident as blood collects and raises ICP. May present with CNIII Palsy and contralateral weakness
161
Q

Where is a subdural haematoma? What does it look like on CT? What causes it? How does it present?

A
  • Between Dura mater and arachnoid marter
  • Looks like a Slither on CT, squashing of ventricle, can be entire length of brain but does not cross due to dural septum
  • Often due to a tear in bridging veins which span the subdural space from a minor fall (elderly)
  • Presents slower than extradural as venous blood. Develops over a period of days to weeks with headache and confusion
162
Q

Where is an subarachnoid haemorrhage? What does it look like on CT? What causes it? How does it present?

A
  • In subarachnoid space between arachnoid mater and pia mater
  • Diffuse white area on CT, often near CoW
  • Caused by a burst berry aneurysm or trauma
  • Rapid onset with severe thunderclap headache, often in occipital region, vomiting, confusion and altered consciousness
163
Q

Where is an intracranial haemorrhage? What does it look like on CT? What causes it? How does it present?

A
  • Within the brain parenchyma
  • Dense white area
  • Haemorrhagic stroke (AV malformation, hypertensive microaneurysm, thrombocytopenia)
  • Depends on location
164
Q

What is diffuse axonal injury?

A

-Acceleration/deceleration within the skull causes shearing of white mater from grey mater presenting as an instant loss of cosciousness and PVS

165
Q

What are the signs of a basal skull fracture?

A
  • Periorbital ecchymosis
  • Mastoid ecchymosis
  • CSF rhinorrhea/otorrhoea
166
Q

What is a coup and contrecoup injury?

A
  • Coup injury is a brain injury caused by site of impact of trauma
  • Contrecoup is a brain injury caused by the brain reverberating from one side of the skull to the other
167
Q

What is the normal ICP? Why can it vary daily?

A
  • 5-15 mmHg

- Changes in arterial and venous pressure

168
Q

What is the monroe-kellie theory?

A
  • The idea that the skull is a fixed closed box with a constant volume made up from venous volume, arterial volume, brain and CSF
  • If one of these volumes increases the other have to decrease to compensate. Venous and CSF compensate first and when they have maximally compensated any increase in volume will directly increase ICP
169
Q

Why does ischaemia occur when ICP rises?

A

-ICP above cerebral perfusion pressure -> vessels vasodilate to decrease pressure -> More blood enters -> rises ICP further -> cannot vasodilate anymore -> blood cannot enter = ischaemia

170
Q

What is the typical history of a raised ICP?

A
  • Headache which is generalised and bilateral
  • Altered mental state
  • NV
  • Worse on laying and first thing in a morning, bending forward and coughing unpleasant
  • Transient uniocular loss of vision
  • Eye signs
171
Q

What eye signs can be seen with raised ICP?

A
  • Papilloedema -> Impaired axoplasmic flow leads to accumulation and optic disc margins become blurred
  • CNIII palsy -> down and out pupil, ptosis and myadriasis -> suggests uncal herniation
  • CNVI palsy -> unable to abduct eye
172
Q

What is the cushings reflex?

A
  • Reflex which occurs as a result of brainstem compression
    1) Increased sympathetic drive causes Increased BP -> decreased carotid baroreceptor firing causes bradycardia. Further compression leads to altered breathing patterns

PPE (15 decks)

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