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PHASE 2A (Mine) > Neuro > Flashcards

Neuro Flashcards

1
Q

What are the 4 lobes of the brain?

A

Frontal lobe
Parietal lobe
Temporal lobe
Occipital lobe

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2
Q

What does is the action of the frontal lobe? (what does it contain?)

A
  • Contralateral motor movement.
  • Broca’s area: Speech and writing
  • Intellectual functioning
  • Thought processing
  • Reasoning
  • Memory
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3
Q

What it the action of the parietal lobe?

A 
Interprets sensation (pain, touch, pressure)
Proprioception
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4
Q

What is the action of the temporal lobe? (what does it contain?)

A

Wernicke’s area: understanding the spoken word

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5
Q

What does the occipital lobe control?

A

Processing visual images

Understanding written words

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6
Q

What is the action of the cerebellum?

A

Receives information from the sensory systems, the spinal cord, and other parts of the brain and then regulates motor movements.
Coordinates voluntary movements such as posture, balance, coordination, and speech.

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7
Q

Draw out the circle of willis:

A

From bottom up:
Basillar artery (with pontine arteries coming off)
Superior cerebellar artery
Posterior cerebral artery
Posterior communicating artery links these to middle cerebral arteries (internal carotids inside this)
Anterior communicating artery links these to anterior cerebral artery

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8
Q

What arteries are responsible for the blood supply to the brain?

A

Internal carotids

Vertebral arteries

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9
Q

Where do the internal carotid arteries originate from?

A

Common carotid arteries which arise (right arises from the brachiocephalic artery- first branch of aorta)

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10
Q

Where do the vertebral arteries originate?

A

Left and right subclavian arteries (right comes off brachiocephalic artery)

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11
Q

What part of the brain does the anterior cerebral artery supply?

A

Anteromedial portion of the cerebrum (middle front)

Supplies motor cortex

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12
Q

What part of the brain does the middle cerebral artery supply?

A

Majority of the lateral part of the brain

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13
Q

What part of the brain does the posterior cerebral artery supply?

A

Medial and lateral parts of the posterior cerebrum . (back of the brain)

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14
Q

What vein do all venous sinuses drain into?

A

Internal jugular vein

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15
Q

What are the main venous sinuses of the brain?

A

Superior sagittal sinus

Inferior sagittal sinus

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16
Q

Where do the 11 venous sinuses of the brain converge?

A

Confluence of sinuses (overlying internal occipital protuberance)

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17
Q

What is the straight sinus a continuation of?

A

The inferior sagittal sinus and great cerebral vein

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18
Q

What happens after the confluence of sinuses?

A

The transverse sinus continues bi-laterally and curves into the sigmoid sinus to meet the opening of the internal jugular vein.

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19
Q

What/ where is the cavernous sinus?

A

Paired dural venous sinus locates on either side of the sella turcica of the sphenoid bone

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20
Q

What structures are in the cavernous sinus?

A 
O TOM CAT
Oculomotor nerve
Trochlear nerve
Opthalmic branch + 
Maxillary branch of trigeminal nerve
Carotid (internal) artery
Abducens nerve
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21
Q

What are the ventricles of the brain and what are they responsible for?

A

Hollow spaces in the middles of the brain, responsible for the porduction, transport and removal of CSF.

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22
Q

What is the fornix of the brain?

A

C-shaped bundle of white matter (nerve fibres) that acts as a major output tract of the hippocampus

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23
Q

What does the fornix connect?

A

2 brain hemispheres, limbic system

Connects hippocampus to mammillary bodies

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24
Q

What is the limbic system of the brain?

A

Set of brain structures involved in behavioural and emotional responses (especially those for survival: feeding, reproduction, fight/flight)

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25
Q

What structures are in the limbic system?

A

Hypothalamus
Amygdala
Thalamus
Hippocampus

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26
Q

What/ where is the hypothalamus?

A

Small region near the pituitary gland that plays an important role in releasing hormones and regulating body temperature

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27
Q

What/ where is the amygdala?

A

Collection of cells near the base of the brain, 1 in each hemisphere.
Responsible for emotional memories (emotions are given meaning and remembred/ given associations)

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28
Q

What/ where is the thalamus?

A

Small structure located just above the brain stem with extensive connections to the cerebral cortex and midbrain.
Primary function is to relay motor and sensory signals to the cerebral cortex.

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29
Q

What/ where is the hippocampus?

A

Structure deep within the temporal lobe of each cerebral cortex.
Principally involved in storing long-term memories.

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30
Q

What is the cerbral cortex?

A

The outer layer of the cerebrum, made up of grey matter.

Contains the 4 lobes

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31
Q

What is the inner layer of the brain?

A

White matter

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32
Q

What is the difference between the grey and white matter of the brain?

A

Grey matter contains cell bodies, dendrites and axon terminals
White matter is made up of myelinated axons, connecting different parts of grey matter to each other.

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33
Q

What is the coronal plane?

A

The frontal plane that separates the front and back

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34
Q

What is the sagittal plane?

A

Longitudinal plane, splits the body left to right.

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35
Q

What is the transverse plane?

A

Horizontal plane, divides the body superiorly and inferiorly

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36
Q

What does rostral mean?

A

Towards the nose

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37
Q

What does caudal mean?

A

Towards the tail

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38
Q

What do dorsal and ventral mean in the brainstem/ spinal cord?

A 
Dorsal= posterior
Ventral= anterior
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39
Q

What do dorsal and ventral mean in the cerebrum?

A 
Dorsal= superior
Ventral= inferior
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40
Q

What are the meninges?

A

The membranous vocerings of the brain and spinal cord

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41
Q

What are the 3 layers of the meninges?

A

Dura mater
Arachnoid mater
Pia mater

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42
Q

Which layer is the dura mater?

A

Outer layer firmly adhered to the inside of the skul?l

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43
Q

Which layer is the arachnoid mater?

A

Middle layer that is more adherent to the brain, keeping CSF in contact with it.

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44
Q

What is the pia mater?

A

Meningeal layer on the surface of the brain that cannot be separated from it (microscopic layer)

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45
Q

What are oligodendrocytes?

A

The myelinating cells of the CNS (produce the insulating sheath on axons)

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46
Q

What are Schwann cells?

A

Type of glial cell that forms the myelin sheath in the peripheral nervous system

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47
Q

What are glial cells?

A

Cells of the nervous system that are non-neuronal (don’t produce electrical impulses)

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48
Q

In what direction are afferent axons signal going?

A

Towards CNS (sensory fibres)

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49
Q

In what direction are efferent signals going?

A

From CNS to another site (motor fibres)

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50
Q

Where is CSF produced?

A

By ependymal cells in the choroid plexuses of the lateral ventricles

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51
Q

What is the passage of CSF?

A

Lateral ventricles–> 3rd ventricle (via intraventricular foramen)–> 4th ventricle (via cerebral aqueduct

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52
Q

How does the CSF connect to the subarachnoid space?

A

From the 4th ventricle via the median foramen of Magendie and two lateral foramen’s of Lushka

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53
Q

What is hydrocephalus?

A

Abnormal accumulation of CSF in the ventricular system (often due to blocked cerebral aqueduct)

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54
Q

What is the autonomic nervous system?

A

System that acts unconsciously to regulate bodily functions.

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55
Q

What is the somatic nervous system?

A

Voluntary nervous system: controls movement

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56
Q

What is the sympathetic nervous system?

A

Fight or Flight section of the autonomic nervous system

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57
Q

What is the parasympathetic nervous system?

A

Rest and digest section of the autonomic nervous system

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58
Q

Where does the sympathetic nervous system leave the CNS?

A

From the thoracic and lumbar regions (T1 - L2)

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59
Q

What is a ganglia?

A

Ovoid structure containing cell bodies of neurons and glial cells supported by connective tissue.
Function like relay stations

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60
Q

What are the sympathetic trunks?

A

Two chains of ganglia on each side of the spinal cord

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61
Q

What neurotransmitter/ receptor type is used at the preganglionic synapses of the sympathetic nervous system?

A

Acetyl-choline (ACh)

Nicotinic receptors

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62
Q

What neurotransmitter is used at the effector synapses of the sympathetic nervous system? (name of receptor?)

A

Noradrenaline

Adrenergic receptors

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63
Q

What amplifies the effects of the sympathetic nervous system?

A

The adrenal glands releasing adrenaline into the blood

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64
Q

What are the main actions of the sympathetic nervous system?

A 
Increases heart rate
Increases force of contractinos
Vasoconstriction
Bronchodilation
Reduces gastric motility
Sphincter contraction
Decreased gastric secretions
Male ejaculation
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65
Q

Where does the parasympathetic nervous system leave the CNS?

A

Brainstem and sacral portion of spinal cord

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66
Q

Where are the preganglionic fibres of the parasympathetic nervous system located?

A

Within 4 nuclei located in the brainstem and associated with a cranial nerves that carry the fibres out of the brain.

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67
Q

Which cranial nerves carry parasympathetic fibres out of the brain?

A

1973:
CN3: Via oculomotor nerve to pupil and facial nerve
CN7: Facial nerve to salivary glands
CN9: Glossopharyngeal nerve for swallowing reflex
CN10: Vagus nerve to thorax and abdomen

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68
Q

What happens to the parasympathetic fibres from each nuclei after they leave the brain?

A

They synapse in a peripheral ganglion and continue to organs in the head and neck

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69
Q

What are the 4 parasympathetic ganglia located within the head?

A

Ciliary

Otic

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70
Q

What do the parasympathetic fibres that leave the CNS at the brainstem supply?

A

Head, neck thorax and abdomen

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71
Q

What do the parasympathetic fibres that leave the CNS at the sacral portion supply?

A

Abdominal and pelvic organs

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72
Q

Where do ganglia usually lie in the parasympathetic nervous system?

A

Within/ very close to the organs that they innervate

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73
Q

What neurotransmitter and receptor is used at the pregnaglion neurone synapse in the parasympathetic nervous system?

A

ACh and nicotinic receptors

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74
Q

What neurotransmitter and receptors are at the effector cell synapse in the parasympathetic nervous system?

A

ACh, muscarinic receptors

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75
Q

What are the main functions of the parasympathetic nervous system?

A 
Decreases heart rate
Decreases force of contraction
Vasodilation
Bronchoconstriction
Increases gastric motility + secretions
Sphincter relaxation
Male erection
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76
Q

What and where is the motor cortex?

A

Region of the frontal lobe responsible for voluntary movement.

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77
Q

Where do the upper motor neurones originate?

A

The motor cortex

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78
Q

Where do the lower motor neurones originate?

A

From upper motor neurones in the brain stem or spinal cord

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79
Q

What is spasticity?

A

When there is an abnormal increase in muscle tone

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80
Q

What is muscle tone?

A

The tension in a muscle at rest

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81
Q

What is rigidity?

A

Increased muscle contraction that is continuous

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82
Q

What is the vertebral column made up of?

A

7 Cervical verterbra
12 Thoracic vertebra
5 lumbar vertebra (fused)
4 coccyx vertebra (fused)

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83
Q

How many spinal nerves are they and how many in each segment?

A 
31
Cervical: 8
Thoracic: 12
Lumbar: 5
Sacral: 5
Coccyx: 1
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84
Q

What is the conus and where does it end?

A

End of the spinal cord that finished before L2

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85
Q

What is the cauda equina?

A

The structure formed by the spinal nerves that arise from the end of the spinal cord bundling together

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86
Q

Where do the spinal nerves originate and together what do they form?

A

From the spinal cord, forming the peripheral nervous system

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87
Q

What does each spinal nerve begin as?

A

An anterior (motor nerve) and posterior (sensory) nerve root

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88
Q

Where do the spinal nerve roots unite to form a single spinal nerve?

A

Interverterbral foramina

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89
Q

What do spinal nerves divide into after leaving the vertebral canal?

A

Posterior and anterior rami

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90
Q

What does the posterior rami supply?

A

Synovial joints of vertebral column, deep muscles of back and overlying skin

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91
Q

What do the anterior rami supply?

A

Remaining area of the body

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92
Q

Where do the spinal nerves of the different sections tend to exit the cord?

A

Cervical: around 1 vertebra higher than they originate
Thoracic: 1-2 vertebra below corresponsing vertebra
Lumbar: 3-4 vertebra blow
Sacral: 5 vertebra below

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93
Q

What is a dermatome?

A

Area of skin supplied by a single sensory spinal nerve

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94
Q

What is the sensory innervation of the hand?

A

Little finger = Ulnar nerve (C8)
Index finger= Median nerve (C7)
Thumb= C6

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95
Q

What is myotome?

A

A volume of muscle supplied by a single spinal nerve

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96
Q

What does the phrenic nerve supply and where does it originate?

A

C3,4,5 keep the diaphragm alive!

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97
Q

What nerves supply the penis?

A

S2,3,4 keeps the penis off the floor

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98
Q

From which direction are all Xrays/ MRI/ CT scans taken?

A

From foot to head

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99
Q

What are ascending tracts?

A

The somatosensory pathways by which SENSORY information from the peripheral nerves is transmitted to the cerebral cortex

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100
Q

What are the two types of ascending tract?

A

Conscious tracts

Unconscious tracts

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101
Q

What are the main ascending tracts?

A

Dorsal column-medial lemniscal pathway
Anterolateral system (spinothalamic tracts)
Spinocerebellar tracts

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102
Q

What does the DCLM pathway carry?

A

Fine touch (tactile) sensation
Vibration
Proprioception

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103
Q

Where does the DCLM tract get its name?

A

Doral column-medial lemniscal pathway:

Travels in the dorsal (posterior) columns and is transmitted through the medial lemniscus in the brain stem.

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104
Q

What neurones are involved in the DCLM pathway?

A

First, second and third order neurones

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105
Q

What do first order neurones do?

A

Carry sensory information from the peripheral nerves to the medulla oblongata.

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106
Q

What are the two pathways that first order neurones can take?

A 
Fasciculus cuneatus (lateral part of dorsal column) - Takes signals from upper limb
Fasciculus gracilis (medial part of dorsal column)- takes signals from lower limb.
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107
Q

Where do the fasciculus cuneatus/ gracilis (first order neurones of DCLM tract) synapse?

A

Nucleus cuneatus/ gracilis of medulla oblongata

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108
Q

What is the action of the second order neurones of the DCLM tract?

A

Deliver information from the first order neurones in the medulla oblongata to the third order neurones in the thalamus.

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109
Q

What do the second order neurones do in the medulla oblongata?

A

Decussate

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110
Q

What is the lemniscus?

A

Bundle of sensory fibres in the brainstem

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111
Q

What do the third order neurones of the DCLM pathway do?

A

Transmit the sensory signals from the thalamus to the ipsilateral primary sensory cortex of the brain, travelling through the internal capsule

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112
Q

What does the anterolateral system consist of?

A

Anterior and lateral spinothalamic tracts

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113
Q

What sensations does the anterior spinothalamic tract carry?

A

Crude touch and pressure

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114
Q

What sensations does the lateral spinothalamic tract carry?

A

Pain and temperature

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115
Q

Where do the first order neurones of the spinothalamic tracts arise and synapse?

A

Arise from sensory receptors in the periphery, ascend 1-2 vertebral levels and synapse at tip of dorsal horn (substantia gelatinosa)

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116
Q

What are the dorsal horns?

A

Where the grey matter, containing cell bodies of sensory neurons, forms two arms at the back of the spinal cord.

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117
Q

Where are the cell bodies for the sensory spinal nerve fibres?

A

Dorsal root ganglion in the dorsal root (Dorsal and ventral root come out of spinal cord before forming spinal nerve)

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118
Q

What is in the centre (‘H’ shape) of the spinal cord?

A

Grey matter containing nerve cell bodies

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119
Q

What surrounds the grey matter of the spinal cord/

A

White matter containing axons (spinal tracts)

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120
Q

Where do the second order neurones of the spinothalamic tract begin and synapse?

A

Carry sensory information from substantia gelatinosa (dorsal horn) to the thalamus

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121
Q

Where do the fibres of the spinothalamic tract decussate?

A

Second order neurones decussate within the spinal cord

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122
Q

What do the second order neurones form after decussating in the spinal cord?

A

Two distinct tracts:
Crude touch and pressure fibres
Pain and temperature fibres

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123
Q

Where do the crude touch and pressure fibres travel up the spinal cord?

A

In the anterior spinothalamic tract

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124
Q

Where do the pain/ temperature fibres travel up the spinal cord?

A

In the lateral spinothalamic tract

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125
Q

Where do the third order neurones of the spinothalamic tract travel?

A

From the thalamus, through the internal capsule to the ipsilateral primary sensory cortex .

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126
Q

What tracts carry unconscious proprioceptive sensation to the brain?

A

Spinocerebellar tracts

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127
Q

What are the 4 pathways in the spinocerebellar tracts?

A

Posterior spinocerebellar tract
Cuneocerebellar tract
Anterior spinocerebellar tract
Rostral spinocerebellar tract

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128
Q

Where do the spinocerebellar tracts carry information to?

A

Ipsilateral cerebellum

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129
Q

What senses do the following carry:

  • DCLM tract
  • Anterior spinothalamic tracts
  • Lateral spinothalamic tract
  • Spinocerebellar tracts
A

DCLM= Proprioception, fine touch and vibration
Anterior spinothalamic= crude touch/ pressure
Lateral spinothalamic= temperature/ pain
Spinocerebellar= unconscious proprioception

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130
Q

What are the descending tracts?

A

Pathways that carry motor signals from the brain to the lower motor neurones

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131
Q

What are the two major groups of the descending tract?

A

Pyramidal tracts

Extrapyramidal tracts

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132
Q

Where do the pyramidal tracts originate?

A

The cerebral cortex

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133
Q

Where do the pyramidal tracts carry motor fibres to?

A

The spinal cord and rain stem

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134
Q

What muscles do the pyramidal tracts control?

A

Voluntary control of body and facial muscles.

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135
Q

Where do the extrapyramidal tracts originate and travel to?

A

Originate in the brain stem and carry fibres to the spinal cord

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136
Q

What is the action of the extrapyramidal descending tracts?

A

Involuntary and autonomic control of all musculature (muscle tone, balance, posture and locomotion)

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137
Q

Are there synapses within the descending pathways?

A

No

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138
Q

Where do the descending pathways synapse?

A

With lower motor neurones at the end of the descending tracts.

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139
Q

What are the neurones of the descending tracts classed as?

A

Upper motor neurones

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140
Q

Where are the upper motor neurone cell bodies located?

A

In the cerebral cortex or brain stem.

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141
Q

Why are they called pyramidal tracts?

A

Because they pass through the medullary pyramids of the medulla oblongata

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142
Q

What are the two pyramidal tracts?

A

Corticospinal

Coricobulbar

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143
Q

What does the corticospinal tract supply?

A

The musculature of the body

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144
Q

Where do the corticospinal tracts begin and where are the inputs from?

A

Begin in the cerebral cortex, with inputs from the:

  • primary motor cortex
  • premotor cortex
  • supplementary motor area
  • somatosensory area
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145
Q

After originating from the cortex, where do the corticospinal neurones convrege and descend through?

A

Internal capsule

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146
Q

What is the internal capsule?

A

A white matter pathway, located between the thalamus and basal ganglia

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147
Q

What makes the internal capsule vulnerable?

A

It is particularly susceptible to compression from haemorrhagic bleeds (capsular stroke)

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148
Q

Where do the neurones pass through after leaving the internal capsule?

A

Crus cerebri of midbrain, pons and medulla.

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149
Q

Where does the corticospinal tract divide into two and what are the two?

A

Divides into the lateral and anterior corticospinal tract in the medulla.

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150
Q

Where do the fibres of the lateral corticospinal tract decussate and terminate?

A

Decussate in the medulla and descend into the spinal cord, terminating at the ventral horn of all segmental levels.

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151
Q

Where do the corticospinal tracts decussate and they terminate?

A

Remain ipsilateral, descend into the spinal cord and then decussate and terminate in the ventral horn of the cervical and upper thoracic segments.

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152
Q

What do the corticobulbar tracts supply?

A

Musculature of the head and neck

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153
Q

Where do the corticobulbar tracts arise?

A

Lateral aspect of the primary motor cortex. (with same inputs as corticospinal tracts)

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154
Q

Where do the fibres converge and travel to?

A

Converge and pass through the internal capsule to the brainstem.

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155
Q

Where to corticobulbar neurones terminate?

A

Motor nuclei of the cranial nerves, where they synapse with lower motor neurones to carry motor signals to the face and neck.

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156
Q

Do the corticobulbar fibres innervate the motor neurones ipsi, contra or bilaterally? What are the exceptions?

A

Bilaterally (both sides no matter where the input is from)

Facial nerve has a ontralateral innervation (affecting muscles in lower quadrant of face)
Hypoglossal nerve is contralateral

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157
Q

What are the extrapyramidal tracts?

A

Descending spinal tracts that carry motor fibres responsible for involuntary and autonomic control of all musculature.

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158
Q

Where to the extrapyramidal tracts originate?

A

The brainstem

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159
Q

What are the 4 extrapyramidal tracts?

A

Vestibulospinal
Reticulospinal
Rubrospinal
Tectospinal

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160
Q

What are the vestibulospinal tracts respondible for and contra or ipsilateral?

A

Responsible for balance and posture

Ipsilateral.

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161
Q

What are the reticulospinal tracts responsible for?

A

Medial: Arises from pons and facilitates voluntary movement and increases muscle tone
Lateral: Arises from medulla and inhibits voluntary movements and reduces muscle tone

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162
Q

What are the rubrospinal tracts responsible for?

A

Uknwon- fine control of hand movements/

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163
Q

Where do the rubrospinal tracts originate and do they decussate?

A

Originate in red nuclues (in midbrain) and decussate, creating contralateral innervation

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164
Q

What are the tectospinal tracts responsible for?

A

Coordinates movements of the head in relation to vision stimuli.

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165
Q

Where do the tectospinal tracts originate and decussate?

A

Superior colliculus of midbrain (recieves input from optic nerves) then decussates and enters the spinal cord.

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166
Q

What is Brown-Sequard syndrome?

A

Damage to one half of the spinal cord (hemisection)

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167
Q

What are potential causes of Brown-sequrd syndrome?

A

Trauma (e.g. knife wound)
Troke
Inflammatory disease (e.g. multiple sclerosis, tuberculosis)

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168
Q

What does Brown-sequard cause?

A

Ipsilateral loss of proprioception, motor and fine touch

Contralateral loss of pain, temperature and crude touch.

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169
Q

What are the cranial nerves?

A 
I: Olfactory
II: Optic
III: Oculomotor
IV: Trochlear (3) 
V: Trigeminal
VI: Abducens
VII: Facial
VIII: Vestibulocochlear
IX: Glossopharyngeal
X: Vagus
XI: Accessory
XII: Hypoglossal
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170
Q

Which cranial nerves are sensory/ motor?

A 
Some 
Say
Marry 
Money 
But 
My
Brother
Says
Big 
Brains
Matter 
More
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171
Q

Which of the cranial nerves are parasympathetic?

A

3,7,9, 10

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172
Q

What is Broca’s area?

A

The language centre of the brain

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173
Q

Where is Broca’s area?

A

Dominant (usually left if right handed) frontal lobe

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174
Q

What is Broca’s area responsible for?

A

Articulation of speech

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175
Q

What does damage to Broca’s area cause?

A

Expressive aphasia: Partial loss of ability to produce language (spoken, manual or written) despite intact comprehension

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176
Q

What is Wernicke’s area?

A

Comprehension centre responsible for understanding speech

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177
Q

Where is Wernicke’s area?

A

Dominant temporal lobe

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178
Q

What does damage to Wernicke’s area cause?

A

Comrehension/ receptive aphasia

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179
Q

What does the external carotid artery supply?

A

Everything in the head and neck except the brain

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180
Q

What will be affected if there is an ischaemic stroke in the anterior cerebral artery?

A

Lower limbs

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181
Q

What will be affected if there is an ischaemic stroke in the middle cerebral artery?

A

Chin to hip

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182
Q

What will be affected if there is an ischaemic stroke in the posterior cerebral artery?

A

Peripheral vision loss

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183
Q

What will be affected if there is an ischaemic stroke in the posterior inferior cerebellar artery?

A

Medulla, resulting in lateral medullay syndrome: dysphagia, slurred speech, ataxia, facial pain, loss of pain/ sensation on opposite side of the body

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184
Q

What are berry aneurysms?

A

Most common type of brain aneurysm that occurs in the circle of Willis

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185
Q

What is an aneurysm?

A

Bulge in a blood vessel caused by a blood vessel wall weakness.

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186
Q

What is the brainstem made up of?

A

Midbrain
Pons
Medulla oblongata

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187
Q

What is the midbrain made up of?

A

Tectum

Cerebral peduncles

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188
Q

What is the substantia nigra?

A

Pigmented nucles (basal ganglia structure) in the midbrain that separates the two cerebral peduncles

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189
Q

What is the tegmentum?

A

Region of grey matter in the midrbain

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190
Q

What is the pons?

A

The largest part of the brainstem, connecting the medulla and midbrain.

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191
Q

What important things does the pons contain?

A

Cranial nerve nuclei

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192
Q

What is the medulla and what does it contain?

A

The lowest part of the brainstem, containing nerve tracts and brainstem nuclei.

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193
Q

What is the action of the cerebellum?

A

Responsible for coordinating voluntary movements.

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194
Q

What is the floor of the cavity made up of?

A

Anterior, middle and posterior cranial fossa

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195
Q

What bones make up the anterior cranial fossa?

A

Frontal
Ehtmoid
Sphenoid

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196
Q

What bones make up the middle cranial fossa?

A

Sphenoid
Temporal
Parietal

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197
Q

What bones make up the posterior cranial fossae?

A

Sphenoid
Parietal
Temporal
Occipital

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198
Q

Where does the spinal cord finish?

A

L1

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199
Q

Where is epidural anaesthetic given and why?

A

In/ around dura mater below L1 so that the brain will still control breathing will the lower body is anaestestised.

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200
Q

How does epidural anaesthetic work?

A

Administered into epidural space and diffuses into dorsal root ganglia on sensory nerves, stopping sensory neurones from working

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201
Q

What is a lumbar puncture?

A

Spinal tap: Very sharp needle inserted to penetrate dura and sample CSF

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202
Q

What are the main diagnostic brain specific tests?

A

Nerve conduction studies
Electromyography
Electroencephalography

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203
Q

What are nerve conduction studies?

A

Look at the peripheral nervous system and assess sensory/ motor function.
Nerve is stimulated with electrodes.

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204
Q

What does it indicate if there is only a small response in a nerve conduction study?

A

There has been axon loss

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205
Q

What does it indicate if there is a slow response in a nerve conduction study?

A

Myelin loss

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206
Q

What is EMG?

A

Electromyography:

Can detect myopathies by recording the electrical activity in skeletal muscles.

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207
Q

What is an EEG?

A

Electroencephalography- tests electrical activity of brain

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208
Q

How do you examine a head injury?

A

Glasgow coma scale
Look at laterlising signs
Look at pupils

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209
Q

What is a stroke?

A

A cerebrovascular accident

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210
Q

What can cause disruption of cerebral blood supply?

A

Thrombus/ embolus (especially in atrial fibrillation)
Atherosclerosis
Shock
Vasculitis

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211
Q

What is a TIA?

A

Transient ischaemic attack: Neurological dysfunction caused by temporary cerebral ischaemia (without infarction)

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212
Q

What time period do TIA symptoms usually resolve within?

A

24 hours

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213
Q

What is a crescendo TIA?

A

Two or more TIAs within a week

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214
Q

What do TIA’s often precede?

A

Full stroke

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215
Q

What are the typical symptoms of a stroke?

A

Sudden onset of asymmetrical:

  • Limb weakness
  • Facial weakness
  • Dysphasia (speech disturbance)
  • Visual/ sensory loss
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216
Q

What are the risk factors for a stroke?

A 
Cardiovascular disease (angina, MI, peripheral vascular disease)
Previous stroke/ TIA
Atrial fibrillation
Carotid artery disease
Hypertension
Diabetes
Smoking
Vasculitis
Thrombophilia
Combined contraceptive pill
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217
Q

What is the pneumonic for recognising a stroke?

A 
FAST:
Face
Arm
Speech
Time (act fast)
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218
Q

What are the two causes of a stroke?

A

Ischaemia/ infarction of brain tissue secondary to inadequate blood supply or
Intracranial haemorrhage.

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219
Q

What is the initial management of a suspected stroke?

A

Exclude hypoglycaemia
Immediate CT to exclude primary intracerebral haemorrhage
Aspirin 300mg stat

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220
Q

How is an ischaemic stroke treated?

A

Thrombolysis with alteplase (thrombolytic medication)

Thrombectomy (mechanical removal of clot) if severe occlusion is confirmed

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221
Q

What are post thrombolysis complications and how are they monitored for?

A

Intracranial or systemic haemorrhage

Repeated CT scans of the brain

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222
Q

How quickly does alteplase have an effect?

A

Within 4.5 hours

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223
Q

Why should blood pressure not be attempted to be lowered during a stroke?

A

To prevent reduced perfusion to the brain

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224
Q

How is TIA managed?

A

Start aspirin 300mg daily
Start secondary prevention measures for cardiovascular disease
Refer to stroke specialist

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225
Q

Why is imaging used in a stroke and what techniques are used?

A

To establish the affected vascular territory:
Diffusion-weighted MRI
CT
Carotid ultrasound (to assess for carotid stenosis)

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226
Q

What is the secondary prevention of stroke?

A

Antiplatelet (clopidogrel)
Statin (Atorvastatin)

Carotid endarterectomy/ stenting in patients with carotid artery disease
Treat modifiable risk factor (e.g. hypertension/ diabetes)

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227
Q

What rehabilitation support might patients who have had a stroke require?

A 
MDT: 
Nurses
Speech and language therapy
Dieticians
Physiotherapy
Occupational therapy
Social services
Optometry/ ophthalmology
Psychology
Orthotics
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228
Q

What percentage of strokes are caused by intracranial bleeds?

A

10-20%

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229
Q

What are the layers between the brain and the skull in order?

A 
Skull
Dura mater
Arachnoid mater
Subarachnoid space
Pia meter
Brain
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230
Q

What is a haemorrhage?

A

Escape of blood from ruptured blood vessel

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231
Q

What are the risk factors for haemorrhagic stroke?

A 
Head injury
Hypertension
Aneurysm
Progression of iscaehemic stroke
Brain tumours
Anticoagulants
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232
Q

How do haemorrhagic strokes present?

A 
Sudden onset headache
Seizures
Weakness
Vomiting
Reduced consciousness
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233
Q

What assessment tool is used to assess consciousness? What is the maximum score?

A

Glasgow coma scale
Max score= 15
Should secure airway if below 8

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234
Q

What is a subdural haemorrhage/ hematoma?

A

Collection of blood in the subdural space (between dura and arachnoid mater)

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235
Q

What causes a subdural haemorrhage?

A

Rupture of the bridging veins in the outermost meningial layet

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236
Q

What is the usually cause of an acute subdural hematoma?

A

External trauma creating tension in the walls of a bridging vein in the subdural space .

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237
Q

What does a subdural haemorrhage look like on a CT scan?

A

Crescent shape not limited by cranial sutures

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238
Q

In what patients do subdural haemorrhage occur more commonly and why?

A

Elderly/ alcoholic patients as they have more atrophy in their brains, making them more likely to rupture.

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239
Q

What are the different types of haemorrhagic stroke?

A

Subdural
Extradural
Intracerebral
Subarachnoid

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240
Q

What is an extradural haemorrhage (epidural hematoma)?

A

Collection of blood between the skull and dura mater.

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241
Q

What is the usual cause of an extradural haemorrhage?

A

Rupture of the middle meningeal artery in the temporo-parietal region, often associated with fracture of the temporal bone

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242
Q

How does an extradural haemorrhage appear on a CT?

A

Bi-convex shape limited by cranial sutures

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243
Q

What is the typical presentation of an extradural haemorrhage?

A

Young patient with a traumatic head injury with ongoing headache. They have a period of improved neurological symptoms and consciousness followed by a rapid decline over hours as the haematoma gets large enough to compress intracranial structures.

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244
Q

What is a subarachnoid haemorrhage?

A

Bleeding into the subarachnoid space (where CSF is located between pia mater and arachnoid membrane)

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245
Q

What is the usual cause of a subarachnoid haemorrhage?

A

Ruptured cerebral aneurysm

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246
Q

What is the typical presentation of an subarachnoid haemorrhage?

A

Sudden onset occipital headache that occurs during strenuous activity (THUNDERCLAP HEADACHE)

Neck stiffness, photophobia, vision changes, neurological symptoms (speech changes, weakness, seizures)

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247
Q

What are the risk factors of a subarachnoid haemorrhage?

A 
Cocaine use
Sickle cell anaemia
Hypertension
Smoking
Excessive alcohol
Family history
Black patients
Females
45-70 y/o
Connective tissue disorders
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248
Q

What are intracerebral haemorrhages?

A

Bleeding into the brain tissue

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249
Q

How does intracerebral haemorrhage present?

A

Similarly to ischaemic stroke

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250
Q

What are the causes of intracerebral haemorrhage?

A

Spontaneous
Result of bleeding into an ischaemic infart
Tumour
Aneurysm rupture

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251
Q

How are haemorrhagic strokes diagnosed?

A

Immediate CT

Check FBC and clotting

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252
Q

How are haemorrhagic strokes managed?

A

Some have surgery to remove blood from the brain/ repair burst blood vessels. (craniotomy)
Correct any clotting abnormality (e.g. stop anticoagulants and give something to reverse it)
Correct severe hypertension
May need supportive treatment: feeding tube/ IV fluids/ ventilation

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253
Q

Why does there need to be a low clinical suspicion to trigger a full investigation os subarachnoid haemorrhage?

A

It has a very high mortality and morbidity.

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254
Q

What investigations are done to diagnose subarachnoid haemorrhage?

A

CT head: hyperattenuation in subarachnoid space
Lumbar puncture (RCC, Xanthochromia- yellow colours CSF)
Angiography to locate source

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255
Q

How is subarachnoid haemorrhage managed?

A

By specialist neurosurgical unit
Patients with reduced consciousness may require intubation and ventilation
Supportive care by MDT team

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256
Q

What interventions may be given to treat subarachnoid hameorrhage?

A

Surgical-> Repair aneurysm by coiling (inserting catherter, placing coil in aneurysm and sealing it off from the artery/ clipping- sealing aneurysm)
Numodipine–> Calcium channel blocker used to treat vasospasm
Lumbar puncture to treat hyercephalus
Antiepileptics to treat seizures

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257
Q

What is hydrocephalus?

A

Accumulation of CSF fluid in the brain, increasing the pressure inside the skull

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258
Q

What is epilepsy?

A

Umbrella term for a condition that causes seizures

259
Q

What are seizures?

A

Transient episodes of abnormal electrical activity in the brain

260
Q

What investigations can be done to diagnose epilepsy?

A

EEG

MRI brain

261
Q

What is an EEG?

A

Electroencephalogram, detects electrical activity in the brain using electrodes.

262
Q

What are the main types of seizure?

A 
Tonic-clonic
Focal
Ansence
Atonic
Myoclonic
Infantile
263
Q

What is a tonic-clonic seizure?

A

Seizure with muscle tensing and jerking.

264
Q

What does tonic mean?

A

Muscle tensing

265
Q

What does clonic mean?

A

Muscle jerking

266
Q

What else may happen in a tonic-clonic seizure?

A

Tongue biting, incontinence, groaning, irregular breathing

267
Q

What happens after a tonic-clonic seizure?

A

Prolonged post-ictal period: person is confused, drowsy and irritable/ depressed

268
Q

How are tonic-clonic seizures managed?

A

First line: Sodium valproate

Second line: Lamotragine/ carbamazepine

269
Q

What are focal seizures?

A

Seizure that starts in one side of the brain

270
Q

What do focal seizures affect?

A

The temporal lobes, affecting hearing, speech, memory and emotions

271
Q

In what ways can focal seizures present?

A 
Hallucinations
Memory flashbacks
Deja vu
Doing strange things on autopilot
Strange feeling
272
Q

What can focal seizures indicate?

A

That another type of seizure is about to happen

273
Q

How are focal seizures treated?

A

First line: Carbamezepine or lamotrigine
Second line: Sodium valproate, levetricetam
(opposite to tonic-clonic)

274
Q

What are absence seizures and in what patients do they usually occur?

A

Typically happen in children. Patients becomes blank, stares into space and is unaware of their surroundings, then abruptly returns to normal after 10-20 seconds.

275
Q

What is the treatment of absence seizures?

A

Sodium valproate or ethosuximide

276
Q

What are atonic seizures?

A

‘Drop seizure’; Brief lapses in muscle tone that lasts less than 3 minutes.

277
Q

What might atonic seizures indicate?

A

Lennox-Gastaut syndome

278
Q

What is the management of atonic seizures?

A

First line: Sodium valproate

Second line: Lamotrigine

279
Q

What are myoclonic seizures?

A

Sudden brief muscle contractions.

280
Q

In what type of epilepsy are myoclonic seizures most common?

A

Juvenile myoclonic epilepsy

281
Q

What is the management of myoclonic seizures?

A

Sodium valproate

Lamotrigine, levetiracetem, topiramate

282
Q

What are infantile spasms?

A

West syndome: Rare disorder starting in infancy that causes clusters of full body spasms and has poor prognosis.

283
Q

What is the first line medication for most forms of epilepsy? What is the exception

A 
Sodium valproate
(Focal seizures the exception)
284
Q

What is the action of sodium valproate?

A

Increases activity of GABA (brain neurotransmitter), which has a relaxing effect on the brain.

285
Q

What is the action of GABA?

A

CNS neurotransmitter that reduces the activity of the neurons to which it binds (inhibits nerve transmission)

286
Q

What are the notable side effects of sodium valproate?

A

Teratogenic
Liver damage and hepatitis
Hair loss
Tremor

287
Q

What does teratogenic mean?

A

Disturbs the development of an embryo/ fetus and may cause birth defects/ miscarriage.

288
Q

In which patients must sodium valproate be avoided?

A

Girls and women unless there are no suitable alternatives and they meet strict criteria that means they do not get pregnant/

289
Q

What is carbamezapine used for and what is its action?

A

First line for focal seizures

Anti-convulsant calcium channel-blocker

290
Q

What are the notable side effects of Carbamazepine?

A 
Agranulocytosis (deficiency of granulocytes) 
Aplastic anaemia (body fails to produce sufficient RBC's) 
Many drug interactions
291
Q

What are the notable side effects of Phenytoin?

A

Folate/ vitamin D deficiency:
Megaloblastic anaemia
Osteomalacia

292
Q

What are the main side effects of ethosuximide?

A

Night terrors

Rashes

293
Q

What is status epilepticus?

A

Medical emergency: Seizures lasting >5 minutes or more that 3 seizures in one hour.

294
Q

How is statues epileptics managed in hospital?

A 
ABCDE
High concentration oxygen
Assess cardiac/ respiratory function
Check blood glucose levels
IV lorazepam (relaxant)
295
Q

What other treatments may be used for epilpesy?

A

Anti-epileptics
Surgery to remove part of the brain causing them
Inserting electrical device to help control them
Ketogenic diet

296
Q

In what aspects of life does epilepsy need to be considered?

A 
Driving
Certain jobs
Swimming
Contraception 
Planning a pregnancy
297
Q

What are the causes of epilepsy?

A 
Idiopathic
Genetic 
Stroke
Brain tumour 
Severe head injury
Drug/ alcohol missure
Brain infection
Lack of oxygen during birth
298
Q

What are the symptoms of a simple focal seizure and why are they called auras?

A 
Remain awake
General strange feeling
Rising sensation in stomach
Deja vu
Unusual smell/ taste
Tingling 
Intense feelings of fear/ joy
Stiffness/ twitching
Can be a sign that another type of seizure is about to happen
299
Q

What are the symptoms of.a complex focal seizure?

A 
Lose sense of awareness and make random body movements such as: 
Smacking lips
Rubbing hands
Random noises
Moving arms 
Chewing/ swallowing
300
Q

What are the two stages of a tonic-clonic seizure?

A
  1. Tonic stage: Lose consiousness and body goes stiff

2. Clonic stage: Limbs jerk, may lose control of bladder or bowel, bite tongue or have difficulty breathing.

301
Q

What can trigger seizures?

A 
Stress
Lack of sleep
Waking up
Alcohol
Some medicines/ drugs
Periods
Flashing lights
302
Q

What is multiple sclerosis?

A

Chronic progressive condition that causes demyleniation of neurones in the CNS/

303
Q

In what patients does MS usually present?

A

Young (<50) women

304
Q

What is the action of myelin?

A

Covers axons of neurons in the CNS to help the electrical impulse move faster.

305
Q

What cells produce myelin?

A

Schwann cells in peripheral nervous system

Oligodendrocytes in CNS.

306
Q

What cells does MS typically affect?

A

Oligodendrocytes - myelin producing cells in the CNS

307
Q

What happens in MS?

A

An inflammatory process is triggered, causing activation of immune cells that damage myelin and affects the way electrical signals travel along the nerve.

308
Q

What can happen in early MS?

A

Re-myelination and resolution of symptoms.

309
Q

What is the characteristic feature of MS?

A

Lesions disseminate in time and space: Lesions vary in their location over time, affecting different nerves and therefore causing different symptoms.

310
Q

What are the predicted causes of MS?

A

Combination of:

  • Specific genetics
  • Epstein-Barr virus
  • Low vitamin D
  • Smoking
  • Obesity
311
Q

How long do symptoms of MS tend to last at first presentation??

A

Progress over more than 24 hours and last days to weeks before improving.

312
Q

In what ways can MS present?

A 
Optic neuritis
Eye movement abnormalities
Focal weakness
Focal sensory symptoms
Ataxia
313
Q

Why are symptoms more permanent in later stage MS?

A

Re-myelination gradually becomes more incomplete

314
Q

What is optic neuritis?

A

Demyelination of the optic nerve and loss of vision in one eye.

315
Q

What eye movement abnormalities might a patient with MS present with?

A

Double vision
Internuclear opthalmoplegia
Conjugate lateral gaze disorder

316
Q

Why might a patient with MS have double vision?

A

Lesions with the sixth cranial nerve (abducens)

317
Q

What do sixth cranial nerve lesions cause?

A

Internuclear opthalmoplegia

Conjugate lateral gaze disorder

318
Q

What is internuclear opthalmoplegia?

A

Problems with the cranial nerve nuclei that control eye movement .

319
Q

What is conjugate lateral gaze disorder?

A

When sixth cranial nerve palsy means that the eyes are unable to move together- the affected eye is unable to abduct/

320
Q

What focal weakness may be present in MS?

A

Bells palsy (paralysis of facial muscles)
Horners syndrome (miosis, ptosis and anhidrosis)
Limb paralysis
Incontinence

321
Q

What focal sensory symptoms may be present in MS?

A

Trigeminal neuralgia
Numbness
Paraesthesia (pins and needles)
Lhermitte’s sign

322
Q

What is Lhermitte’s sign?

A

An electric shock sensation that travels down the spine and limbs when flexing the neck, caused by stretching the demyelinated dorsal column.

323
Q

What is ataxia?

A

Problem with coordinated movement

324
Q

What is sensory ataxia?

A

Loss of proprioceptive sense (can’t sense position of joint), resulting in a positive Romberg’s test

325
Q

What is Romberg’s test?

A

Test of the bodys sense of proprioception. (involves counting seconds patient is able to stand still with eyes closed).

326
Q

What key sign might sensory ataxia cause?

A

Pseudoathetosis- abnormal writhing of the fingers.

327
Q

What is cerebellar ataxia?

A

Problems with the cerebellums coordination of movement.

328
Q

What disease patterns can MS cause?

A

Mild relapsing-remitting episodes for life
Primary progressive MS
Secondary progressive
Clinically isolated syndrome

329
Q

What is clinically isolated syndrome?

A

The first episode of demyelination and neurological signs and symptoms. Cannot diagnose MS until a second instance has occured but patients may only have this one episode

330
Q

What is the most common pattern of MS at initial diagnosis?

A

Relapse-remitting:

Can be active, non-active, worsening or not-worsening

331
Q

What is secondary progressive MS?

A

Where there was relapsing-remitting disease at first, but now there are progressive worsening of symptoms with incomplete remissions.

332
Q

What can secondary progressive MS be further classified as?

A

Active: new symptoms developing/ new lesions on MRI
Not active: No new symptoms/ lesions
Prgressing: Overall worsening of disease over time
Not progressing

333
Q

What is primary progressive MS?

A

When there is a worsening of disease and neurological symptoms from the point of diagnosis without initial relapses and remissions.

334
Q

How is MS diagnosed?

A

Made by neurologist based on clinical picture and symptoms suggesting lesions change location over time.

335
Q

What is required for a diagnosis of primary progressive MS?

A

Symptoms to have been progressive over a period of 1 year.

336
Q

What investigations can support a diagnosis of MS?

A

MRI scans

Lumbar puncture can detect oligoclonal bands in CSF

337
Q

What is optic neuritis?

A

Unilateral reduced vision developing over hours-days

338
Q

What are the key features of optic neuritis?

A

Central scotoma (enlarged blind spot)
Pain on eye movement
Impaired colour vision
Relative afferent pupillary defect

339
Q

How is optic neuritis treated?

A

Steroids

340
Q

How is MS managed?

A

By MDT team with disease- modifying drugs and biologic therapy

341
Q

How are MS relapses treated?

A

Steroids (methylprednisolone):
500mg orally for 5 days
OR 1g IV for 3-5 days

342
Q

What are symptomatic treatments of MS?

A

Exercise to maintatin activity and strength
Amitriptyline/ Gabapentin for neuropathic pain
SSRI’s for depression
Anticholinergics for urge incontinence
Gabapentin/ physio for spasticity

343
Q

What are the main symptoms of MS?

A 
Fatigue
Difficulty walking
Vision problems
Incontinence
Numbness/ tingling
Muscle stiffness/ spasms
Problems with balance/ coordination
Problems thinking/ learning/ planning
344
Q

What is motor neurone disease?

A

Progressive, ulimately fatal disease where the motor neurones stop functioning.(encompasses a variety of specific diagnoses)

345
Q

What is the most common type of MND?

A

Amylotropic lateral sclerosis (AML)

346
Q

What are the main types of motor neurone disease?

A

AML
Progressive bulbar palsy
Progressive muscular atrophy
Primary lateral sclerosis

347
Q

What muscles does progressive bulbar palsy primarily affect?

A

Muscles of talking and swallowing.

348
Q

What is the cause of motor neurone disease?

A

Unknown

Linked to genes, family history, smoking, exposure to heavy metals and certain pesticides.

349
Q

Which neurones are affected in motor neurone disease?

A

Upper and lower motor neurones (not sensory)

350
Q

What patient is the typical presentation of motor neurone disease?

A

Late middle aged man (e.g. 60), possible with affected relative.

351
Q

What are the main symptoms of motor neurone disease?

A

Insidious (gradual), progressive weakness of the muscles throughout the body affecting the limbs, trunk, face and speech.

352
Q

Where is muscle weakness usually first noticed in MND?

A

Upper limbs

353
Q

What other symptoms (other than muscle weakness) may MND patients complain of?

A 
Increased fatigue when exercising
Clumsiness
Dropping things
Tripping over
Slurred speech (dysarthria)
354
Q

What are the key signs of lower motor neurone disease?

A

Muscle wasting
Reduced tone
Fasciculations (muscle twitches)
Reduced reflexes

355
Q

What are the key signs of upper motor neurone disease?

A

Increased tone/ spasticity
Brisk reflexes
Upgoing plantar responses

356
Q

What is spasticity?

A

Abnormal increase in muscle tone (stiffness of muscle)

357
Q

How is MND diagnosed?

A

Based on clinical presentation and excluding other conditions (made by a specialist when there is certainty)

358
Q

How can MND be managed?

A

No effective treatments for halting or reversing progression.
Riluzole can slow progression
Edaravone
Non-invasive ventilation to support breathing at night.

359
Q

What is Parkinson’s disease?

A

Condition where there is a progressive reduction of dopamine in the basal ganglia of the brain, leading to disorders of movementq

360
Q

What is the classic triad of features in Parkinsons?

A

Resting tremor
Rigidity
Bradykinesia

361
Q

What is bradykinesia?

A

Slowness of movement

362
Q

What are the basal ganglia?

A

Group of nuclei in the middle of the brain, responsible for coordinating habitual movements such as walking or looking around.

363
Q

Who is the typical patient presenting with Parkinsons?

A

Older man around 70.

364
Q

What are the key symptoms/ signs of Parkinsons?

A 
Unilateral tremor 
Rigidity
Bradykinesia
Stooped posture
Facial masking
Forward tilt
Reduced arm swing
Shuffling gait
365
Q

What is the frequency of a Parkinsons tremor?

A

4-6 Hz (occurs 4-6 times a second)

366
Q

What does a Parkinsons tremor look like?

A

Pill rolling tremor- looks like rolling pill between fingertips and thumb.
More pronounced when resting or patient is distracted.

367
Q

What is rigidity?

A

Resistance to passive movement of a joint (e.g. will feel tension if trying to flex and extend elbow)

368
Q

What kind of rigidity is experienced in Parkinson’s patients?

A

Cogwheel rigidity- tension in the arm gives way to movement in small increments

369
Q

Whats the difference between spasticity and rigidity?

A

Spasticity arises as a result of daage to the corticoreticulospinal (pyramidal) tracts
Rigidity is caused by dysfunction of extrapyramidal pathways (basal ganglia)

370
Q

In what ways can bradykinesia present?

A

Handwriting gets smaller
Shuffling gait (can only take small steps)
Difficulty initiating movement
Difficulty in turning around when standing
Reduced facial movement and facial expressions

371
Q

What other features can effect patients with Parkinsons?

A 
Depression
Sleep disturbance/ insomnia
Loss of sense of smell (anosmia) 
Postural instability
Cognitive impairment/ memory problems
372
Q

How is a benign essential tremor differentiated from a Parkinson’s tremor?

A

Benign essential is:
Symmetrical
5-8 Hz (instead of 4-6)
Improves at rest (P gets worse)
Worse with intentional movement (P improves)
No other Parkinson’s features
Improves with alcohol (P has no change with alcohol)

373
Q

What are Parkinson’s plus syndromes?

A

Atypical Parkinson’s- Diseases that are linked to Parkinson’s and cause a lot of the same symptoms but can bring other problems

374
Q

What is multiple system atrophy?

A

Rare condition where the neurones of multiple systems in the brain degenerate

375
Q

How does multiple system atrophy present?

A

Degeneration in basal ganglia leads to Parkinson’s presentation, degeneration in other areas leads to autonomic dysfunction (postural hypotension, constipation, abnormal sweating, sexual dysfunction) and cerebellar dysfunction (ataxia)

376
Q

What are some examples of Parkinson’s plus syndromes?

A

Multiple system atrophy
Dementia with Lewy bodies
Progressive supranuclear palsy
Corticobasal degeneration

377
Q

How is Parkinson’s diagnosed?

A

Clinically based on symptoms and examination

378
Q

What produces dopamine?

A

Substantia nigra of the basal ganglia in the midbrain.

379
Q

What is dopamine essential for?

A

The correct functioning of the basal ganlia.

380
Q

What happens to Dopamine levels in Parkinsons?

A

There is a gradual but progressive fall in production

381
Q

What medications are used control symptoms of Parkinsons?

A

Levodopa
COMT inhibitors
Dopamine agonists
Monoamine Oxidase-B inhibitors

382
Q

What is Levodopa?

A

Synthetic dopamine given orally to boost dopamine levels

383
Q

What does Levodopa need to be given with?

A

Peripheral decarboxylase inhibitors (e.g. Carbidopa and benserazide) that stop levodopa being broken down by the body before it can enter the brain.

384
Q

Why is Levopoda treatment reserved for when other treatments are not managing to control symptoms?

A

It becomes less effective over time

385
Q

What is the main side effect of dopamine treatment?

A

If the dose is too high, develop dyskinesias (abnormal movements associated with excessive motor activity)

386
Q

What are some examples of dyskinesias?

A

Dystonia (abnormal postures/ exaggerated movements)
Chorea (abnormal involuntary movements-jerking)
Athetosis (involuntary twisting/ writhing movements in hands, fingers or feet)

387
Q

What are COMT inhibitors? (+ example)

A

Inhibitors of COMT enzyme which metabolises levodopa in the body and brain (e.g. entacapone)/ Is taken to slow breakdown of levodopa in the brain, extending its effects

388
Q

What are dopamine agonists actions?

A

Mimic dopamine in the basal ganglia and stimulate dopamine receptors.

389
Q

How effective are dopamine agonists and what is their main side effect?

A

Less effective than Levopoda

Can cause pulmonary fibrosis

390
Q

What are monoamine oxidase-B inhibitors?

A

Monoamine oxidase enzymes break down neurotransmitters, and B is specific to dopamine. Therefore inhibitors block this enzyme and increase circulating dopamine.

391
Q

What causes neuropathic pain?

A

Abnormal functioning of the sensory nerves delivering abnormal and painful signals to the brain

392
Q

What are the typical features of neuropathic pain?

A 
Burning 
Tingling
Pins & needles
Electric shock
Loss of sensation
393
Q

What can cause neuropathic pain?

A 
Nerve damage from surgery
Multiple sclerosis
Diabetes neuralgia
Trigeminal neuralgia
Complex regional pain syndrome
Postherpetic neuralgia from shingles
394
Q

What is used to assess neuropathic pain?

A

DN4 questionaire

395
Q

What are the 4 first line treatments for neuropathic pain?

A

Amitriptyline (Tricyclic antidepressant)
Duloxetine (SNRI antidepressant)
Gabapentin (antivonvulsant)
Pregabalin (anticonvulsant)

396
Q

What is trigeminal neuralgia and what is used to treat it?

A

Chronic pain condition affecting the trigeminal nerve of the face and brain.
Treated with carbamexepine

397
Q

Where does the facial nerve exit the brainstem?

A

At the cerebellopontine angle

398
Q

What branches does the facial nerve divide into?

A 
Temporal 
Zygomatic
Buccal
Marginal mandibular
Cervical
(Tall zulus bear many children)
399
Q

What sensory function does the facial nerve carry?

A

Taste from the anterior 2/3 of the tongue

400
Q

What will happen to the forehead in an upper motor neurone lesion?

A

The forehead will be spared and can be moved on the affected side

401
Q

What will happen to the forehead in a lower motor neurone lesion?

A

The patient cannot move the forehead on the affected side.

402
Q

How do brain tumours present?

A

Usually asymptomatic

As they develop, present with focal neurological symptoms, and signs and symptoms of raised intracranial pressure

403
Q

What are the main causes of raised intracranial pressure?

A 
Brain tumour
Intracranial haemorrhage
Idiopathic intracranial hypertension
Abscess
Infection
404
Q

How does raised intracranial pressure present?

A 
Headache that is: 
-Constant
-Nocturnal
-Worse on waking, coughing, straining or bending forward
Vomiting
Altered mental state
Visual field defects
Unilateral ptosis
3/6 nerve palsies
405
Q

What is the key finding on fundoscopy when assessing for raised intracranial pressure?

A

Papilloedema- Swelling of the optic disc.

406
Q

What are the different types of brain tumour?

A 
Secondary metastases
Gliomas
Meningiomas
Pituitary tumours
Acoustic neuroma
407
Q

What are the most common cancers the metastasise to the brain?

A

Lung
Breast
Renal cell carcinoma
Melanoma

408
Q

What are gliomas?

A

Tumours of the glial cells in the brain or spinal cord

409
Q

What are glial cells?

A

Non-neuronal cells in the CNS (maintain homeostasis, form myelin and provide support/ protection) e.g. schwann cells, oligodendoryctes, astrocytes, ependymal cells

410
Q

What are the three main types of glioma? (most to least malignant)

A

Astrocytoma
Oligodendroglioma
Ependymoma

411
Q

How are gliomas graded?

A

From 1-4
1= most benign
4= Most malignant

412
Q

What is the most malignant type of brain cancer?

A

Glioblastoma

413
Q

What are meningiomas?

A

Tumours growing from cells of the meninges in the brain and spinal cord.

414
Q

How bad are meningiomas/

A

Usually benign, but take up space and can therefore lead to raised intracranial pressure and neurological symptoms

415
Q

Are pituitary tumours usually benign or malignant and what is their main effects?

A

Usually benign but can press on optic chiasm to cause bitemporal hemionopia
May also cause hormone deficiencies of release excessive hormones leading to endocrine disorders

416
Q

What is bitemporal hemianopia?

A

Loss of the outer half of the visual fields in both eyes

417
Q

What are the main endocrine disorders pituitary tumours can cause?

A

Acromegaly
Hyperprolactinaemia
Cushing’s disease
Thyrotoxicosis

418
Q

What are acoustic neuromas?

A

(Vastibular Schwannoma) Tumours of the Schwann cells surrounding the auditory nerve that innervate the inner ear.

419
Q

Where do acoustic neuromas usually occur and are they unilateral?

A

Around the cerebellopontine angle and are usually unilateral

420
Q

What are the classic symptoms of acoustic neuroma?

A

Hearing loss
Tinnitus
Balance problems

421
Q

What are the management options of brain tumours?

A

Palliative care
Chemotherapy
Radiotherapy
Surgery: Depends on grade and behaviour of tumour

422
Q

What are the treatment options of pituitary tumours?

A

Trans-sphenoidal surgery
Radiotherapy
Bromocriptine to block prolactin-secreting sumours
Somatostatin analogues to block GH secreting tumours

423
Q

What is Huntingdon’s disease?

A

Autosomal dominant genetic condition that causes progressive deterioration of the nervous system

424
Q

At what age do symptoms of Huntingdon’s begin to present?

A

30-50

425
Q

What is the inheritance pattern of Huntingdon’s?

A

Autosomal dominant

Trinucleotide repeat disorder: genetic mutation in the HTT gene on chromosome 4.

426
Q

What are trinucleotided repeat disorders?

A

Group of disease caused by a mutation in which repeats of three nucleotides increase in copy numbers and affect the nervous system.

427
Q

What is the main features of trinucleotide repeat disorders?

A

Anticipation: Where successive generations have more repeats in the gene, resulting in earlier age of onset and increased severity

428
Q

How does Huntingdon’s typically initially present?

A

Cognitive, psychiatric or mood problems

429
Q

What are the physical symptoms of Huntingdon’s?

A

Chorea
Eye movement disorders
Dysarthria (Speech difficulties)
Dysphagia (swallowing difficulties)

430
Q

What is chorea?

A

Involuntary, abnormal movements

431
Q

How is Huntingdon’s diagnosed?

A

Specialist genetic centre using a genetic test.

432
Q

What are the key management steps in Huntingdon’s?

A 
No treatment options:
MDT team
Speech/ language therapy
Genetic counselling
Advance directive/ end of life care planning
433
Q

What medicines can be used to help with the symptoms of Huntingdon’s?

A

Ones to supress disordered movement (antipsychotics, Benzodiazepines, dopamine-depleting agents)
Antidepressants

434
Q

What is the prognosis of Huntingdons?

A

Life expentancy is 15-20 years after the onset of symptoms.

435
Q

What is the usual cause of death in Huntingdon’s?

A 
Respiratory disease (pneumonia)
Suicide
436
Q

What are the differential diagnoses of headaches?

A 
Tension headache
Migraine
Cluster headaches
Secondary headaches
Sinusitis
Giant cell arteritis
Glaucoma
Intracranial haemorrhage
Subarachnoid haemorrhage
Anaelgesic headache
Hormonal headache
Cervical spondylosis
Trigeminal neuralgia
Raised intracranial pressure
Meningitis
Encephalitis
437
Q

What red flags should be looked for when assessing headache?

A

Fever, photophobia or neck stiffness (Meningitis/ encephalitis)
New neurological symptoms (haemorrhage, malignancy, stroke)
Dizziness (stroke)
Visual disturbance (temporal arteritis/ glaucoma)
Sudden onset occipital headache ( subarachnoid haemorrhage)
Worse on coughing/ straining/ bending over (raised intracranial pressure)
Severe enough to wake from sleep
Vomiting
History of trauma
Pregnancy

438
Q

What is an important examination when assessing headache?

A

Fundoscopy to look for raised intracranial pressure

439
Q

What are tension headaches?

A

Mild ache across forehead and around head in band like pattern

440
Q

What are tension headaches caused by?

A

Muscle ache in the frontalis, temporalis and occipitalis muscles

441
Q

What are the associated causes of tension headaches?

A 
Stress
Depression
Alcohol
Skipping meals
Dehydration
442
Q

How are tension headaches treated?

A

Basic analgesia
Relaxation techniques
Resolve on their own

443
Q

What are secondary headaches?

A

Similar presentation to tension headaches but with clear cause

444
Q

What may cause a secondary headache?

A

Underlying medical condition (infection, obstructive sleep apnoea, pre-eclampsia)
Alcohol
Head injury
Carbon monoxide poisoning

445
Q

What is sinusitis?

A

Headache associated with inflammation in the ethmoidal, maxillary, frontal or sphenoidal sinuses.

446
Q

What is an analgesic headache?

A

Headache caused by long term analgesia use.

447
Q

What is a hormonal headache?

A

Headache related to low oestrogen (e.g. during/ before period, menopause and pregnancy)

448
Q

What is cervical spondylosis?

A

Condition caused by degenerative changes in the cervical spine. Causes neck pain and often presents with headache.

449
Q

What are the three branches of the trigeminal nerve?

A

Opthalmic (V1)
Maxillary (V2)
Mandibular (V3)

450
Q

What is trigeminal neuralgia?

A

Intense spontaneous facial pain caused by the trigeminal nerve

451
Q

How is trigeminal neuralgia treated?

A

Carbamazepine

452
Q

What is Myasthenia gravis?

A

Autoimmune condition that causes muscle weakness

453
Q

What age does myasthenia graves usually present?

A

Women: under 40
Men: Over 60

454
Q

What other condition does Myesthenia gravis have links to?

A

Thymoma (thymus gland tumour)

455
Q

What goes wrong in Myasthenia gravis?

A

ACh receptor antibodies are produced by the immune system, which bind to postsynaptic neuromuscular junction receptors and block them. This prevents acetylcholine from being able to stimulate the receptor and trigger muscle contraction.

456
Q

Why does weakness get worse with activity and better with rest in Myasthenia gravis?

A

More and more receptors get blocked up as the receptors are used more during muscle activity.

457
Q

What other action do the AcH antibodies perform, making symptoms worse?

A

Activate the complement system, causing damage to postsynaptic membrane cells

458
Q

How does Myasthenia gravis present?

A 
(Varies drastically)
Weakness that gets worse with muscle use and improves with rest:
Douple vision
Ptosis (eyelid drooping) 
Facial drooping
Difficulty swallowing
Jaw fatigue when chewing
Slurred speech
459
Q

What examinations can be done to assess Myasthenia gravis?

A

Repeated blinking
Prolonged upwards gazing (will exacerbate diplopia on further testing)
Repeated abduction of one arm 20 times will result in unilateral weakness
Check for thymectomy scar
Test FVC

460
Q

How can Myasthenia gravis be diagnosed?

A

Testing for antibodies (ACh-R antibodies, MuSK, LRP4)
CT/ MRI of thymus to look for thymoma
Edrophonium test

461
Q

What is the edrophonium test?

A

IV dose of edrophonium chloride given, which blocks enzymes which breakdown ACh. This will increase the level of ACh at the neuromuscular junction and briefly relieve weakness, establishing diagnosis

462
Q

What are the treatment options for Myasthenia gravis?

A

Reversible acetylcholinesterase inhibitors
Immunosuppression
Thymectomy
Monoclonal antibodies (Rituximab, Eculizumab)

463
Q

What is the most severe complication of Myasthenia gravis?

A

Myasthenic crisis: acute worsening of symptoms often triggered by another illness. Can lead to respiratory failure due to muscle weakness.

464
Q

What is Lambert-Eaton myasthenic syndrome?

A

Similar features to Myasthenia gravis but caused by small-cell lung cancer producing antibodies which damage voltage-gated calcium channels.

465
Q

What is Charcot-Marie-Tooth disease?

A

Inherited disease that affects the peripheral motor and sensory nerves by causing dysfunction in the myelin or axons

466
Q

What is the usualy inheritance pattern in Charcot-Marie-Tooth disease?

A

Autosomal dominant

467
Q

What are the classical features of Charcot-Marie-Tooth disease?

A 
High arches
Distal muscle wasting
Weakness in lower legs and hands
Reduced tendon reflexes
Reduced muscle tone
Peripheral sensory loss
468
Q

What are the other causes of peripheral neuropathy (other than Charcot-Marie-Tooth disease)?

A 
Alcohol
B12 deficiency
Cancer/ chronic disease
Diabetes/ drugs
Every vasculitis
469
Q

How is Charcot-Marie-Tooth disease?

A

Not treatment

Supportive management

470
Q

What is Guillain-Barre syndrome?

A

Acute paralytic polyneuropathy

471
Q

What is Guillain-Barre syndrome usually triggered by?

A

Infection (Campylobacter jejuni, cytomegalovirus, EBV)

472
Q

What is the cause of Guillain-Barre syndrome?

A

Molecular mimcry: B cells of the immune system create antibodies against antigens on the pathogen that cause the preceding infection. These match proteins on nerve cells and may target proteins on the myelin sheath or axon of motor nerve cells.

473
Q

How does Guillain-Barre syndrome present?

A
  • Acute, symmetrical ascending weakness
  • Reduced reflexes
  • Peripheral loss of sensation or neuropathic pain
  • May progress to cranial nerves and cause facial nerve weakness
474
Q

What is the typical disease course in Guillain-Barre syndrome?

A

Symptoms start within 4 weeks of preceding infection, starting in the feet and progressing upwards.
Symptoms peak within 2-4 weeks, then recovery lasts months to years

475
Q

How is Guillain-Barre syndrome diagnosed?

A

Brighton criteria
Nerve conduction studies (reduced signals)
Lumbar puncture for CSF (raised protein)

476
Q

How is Guillain-Barre syndrome managed?

A

IV immunoglobulins
Plasma exchange
Supportive care
VTE prophylaxies

477
Q

What is the prognosis of Guillain-Barre syndrome?

A

80% fully recover
15% left with neurological disability
5% die

478
Q

What are migraines?

A

Complex neurological condition that cause headache and associated symtpoms

479
Q

What are the different types of migraine?

A

Migraine without aura
Migraine with aura
Silent migraine (aura but no headache)
Hemiplegic migraine

480
Q

What are the typical headache symptoms associated with migraines?

A 
Last between 4-72 hours
Moderate to severe intensity
Pounding/ throbbing
Usually unilateral
Photophobia
Phonophobia
With or without aura
Nausea/ vomiting
481
Q

What is aura?

A 
Visual changes associated with migraines:
Sparks in vision
Blurred vision
Lines in vision
Loss of visual fields
482
Q

What is a hemiplegic migraine?

A

Mimic stroke:
Headache with weakness on one side of the body (hemiplegia), ataxia (slurred speech, loss of coordination etc) and changes in consciousness

483
Q

What are potential migraine triggers?

A 
Stress
Bright lights
Strong smells
Certain foods
Dehydration
Menstruation
Abnormal sleep
Trauma
484
Q

What are the 5 stages of a migraine?

A
  1. Premonitory/ prodromal stage (up to 3 days before)
  2. Aura (lasting <60 mins)
  3. Headache (4-72 hours)
  4. Resolution
  5. Postdromal/ recovery phase
485
Q

What is the acute management of migraines?

A 
Sleep
Paracetamol
Triptans
NSAIDs
Antiemetics
486
Q

What are Triptans?

A

5HT (seretonin) receptor agonists used to abort migraines when they begin

487
Q

What can be used as migraine prophylaxis?

A

Avoid triggers
Certain medications (propanolol, topiramate, amitryptyline)
Acupuncture
B12

488
Q

What are cluster headachers?

A

Severe unbearable unilateral headache, usually around the eye

489
Q

Why are they called cluster headaches?

A

Come in clusters of attacks (e.g. 3-4 attacks a day for weeks/ months followed by 1-2 pain free years)

490
Q

How long do cluster headache attacks typically last?

A

15 mins- 3 hours

491
Q

Who is a typical patient presenting with cluster headaches?

A

30-50 year old male smoker

492
Q

What are the symptoms of cluster headaches?

A 
Severe intolerable unilateral headaches
Red, swollen watering eye
Pupil constriction (miosis)
eyelid drooping (ptosis)
Nasal discharge
Facial sweating
493
Q

How are cluster headachers managed?

A

Triptans

High flow oxygen

494
Q

What is meningitis?

A

Inflammation of the meninges (brain/ spinal cord lining) due to bacterial of viral infection

495
Q

What are the most common causes of bacterial meningitis and what kind are they?

A 
Neisseria meningitidis (gram negative diploccous)--> (also known as MENINGOCOCCUS)
Strep. Pneumoniae (PNEUMOCOCCUS)
Neonates= Group B Streptococcus
496
Q

What is meningococcal septicaemia?

A

When the meningococcus bacterial infection is in the bloodstream

497
Q

What common symptom does meningococcal septicaemia cause?

A

Non-blanching rash

498
Q

What is meningococcal meningitis?

A

When the bacteria is infecting the meninges and CSF

499
Q

What are the typical symptoms of meningits?

A 
Fever
Neck stiffness
Vomiting
Headache
Photophobia
Altered consciousness
Seizures
(may be non-blanching rash)
500
Q

How do neonates present with meningitis?

A

Non-specific signs:

Hypotonia, poor feeding, lethargy, hypothermia, bulgin fontanella, fever

501
Q

What tests can be done to look for meningeal irritation?

A

Kernig’s test: Stretching meninges to look for pain/ resistance to movement
Brudzinski’s test: Lifting head/ neck off bed and flexing chin to see if there is involuntary flexing of hips and knees

502
Q

How is bacterial meningitis managed in the community?

A

Urgent stat injection of benzylpenicillin prior to transfer to hospital

503
Q

How is bacterial meningitis diagnosed in hospital?

A

Lumbar puncture for CSF
Blood tests for meningococcal PCR
(low threshold for treatment)

504
Q

How is bacterial meningits treated in hospital?

A

<3 months: Cefotaxime + amoxicillin
>3 months Ceftriaxone
Vancomycin if there is risk of penicillin resistant infection
Steroids to reduce severity/ frequency of hearing loss/ neurological damage
Dexamethasone

505
Q

Who should be told about bacterial meningitis/ meningococcal infection?

A

Notifiable diseases so public health needs to be notified

506
Q

What is given to people who have been in contact with a meningitis patient within 7 days of the illness onset?

A

Post exposure prophylaxis with ciproflocaxin

507
Q

What are the most common causes of viral meningitis?

A

Herpes simplex
Enterovirus
Varicella zoster virus (VZV)

508
Q

Is Viral meningitis worse or better than bacterial and how is it treated?

A

Milder and often only requires supportive treatment

509
Q

What is a lumbar puncture?

A

Inserting a needle into the lower back to collect a sample of CSF

510
Q

What can be analysed for in CSF sample?

A 
Bacterial culture
Viral PCR
Cell count
Protein 
Glucose
511
Q

What are the characteristics of CSF in a bacterial infection?

A 
Cloudy
High protein count (Bacteria release them)
Low glucose (bacteria use it up)
High white cell count (neutrophils)
Bacterial culture
512
Q

What are the characteristics of CSF in a viral infection?

A 
Clear
Normal protein count
Normal glucose
High white cell count (lymphocytes)
Negative culture
513
Q

What are the key complications of meningitis?

A

Hearing loss
Seizures/ epilepsy
Cognitive impairment/ learning disability
Memory loss
Focal neurological deficits( (limb weakness, spasticity)

514
Q

What is encephalitis?

A

Inflammation of the brain (can be infective or non-infective)

515
Q

What is the most common cause of encephalitis?

A

Viral- Herpes simplex virus

VZV, EBV, Influenza

516
Q

How does encephalitis present?

A 
Altered consciousness
Altered cognition
Unusual behaviour
Acute onset of focal neurological symptoms
Acute onset of focal seizures
Fever
517
Q

How is encephalitis diagnosed?

A 
Lumbar puncture (for viral PCR)
CT scan
MRI
EEG recording
Swabs
HIV testing
518
Q

How is encephalitis managed?

A 
IV antivirals (e.g. Aciclovir) 
Repeat lumbar puncture to ensure successful treatment
519
Q

What are the main complications of encephalitis?

A 
Lasting fatigue
Change in personality/ mood/ memory/ cognition
Learning disability
Headaches
Chronic pain
Movement disorders
Sensory disturbance
Seizures
Hormonal imbalance
520
Q

What is the most common cause of dementia?

A

Alzheimer’s disease

521
Q

What is dementia?

A

Syndrome associated with progressive decline of brain function, including memory, language and problem-solving abilities

522
Q

What might dementia symptoms include?

A 
Memory loss
Slow processing
Language/ speaking problems
Problems with understanding/ judgement
Mood changes
Difficulty doing daily activities
Hallucinations
523
Q

How common is dementia?

A

1 in 6 people over 80 has it

524
Q

What are the different types of dementia?

A 
Alzheimer's
Vascular dementia
(Combination/ Mixed)
Lewy body
Frontotemporal
525
Q

What are most causes of dementia associated with?

A

Abnormal build-up of proteins in the brain, causing neurones to lose function and ultimately die, causing areas of the brain to shrink

526
Q

What causes Alzheimer’s?

A

Abnormal build up of two proteins: amyloid and tau

527
Q

What does builup of amyloid do in the brain?

A

Deposits as plaques around brain cells

528
Q

What do deposits of tau form. inthe brain?

A

Tangles

529
Q

What does Alzheimer’s do to neurotransmitter levels?

A

Decreases, especially ACh

530
Q

What are the risk factory for Alzheimer’s?

A 
Increasing age
Family history
Untreated depression
Cardiovascular disease risk factors (e.g. smoking, obesity, diabetes)
Down's syndrome
Head injuries
531
Q

How is Alzheimer’s diagnosed?

A

Rule out other causes
Questionnaires/ memory / mental ability tests
CT/ MRI

532
Q

What can worsen the symptoms of dementia?

A

Infections
Stroke
Delirium
Certain medicines

533
Q

What are the 3 main stages of Alzheimer’s?

A 
Early symptoms (memory lapses)
Middle-stage symptoms (Worsening memory with changes to behaviour)
Later symptoms (increasingly severe symptoms, including hallucinations and delusions)
534
Q

What medicines can be given to help manage alzheimer’s?

A

Acetylcholinesterase (AChE) inhibitors: Increase levels of acetylcholine
Memantine: Blocks effects of excessive glutamate

535
Q

What is BPSD?

A 
Behavioural and psychological symptoms of dementia: e.g.
Increased agitation
Anxiety
Wandering
Aggression
Delusions/ hallucinations
536
Q

What can be given to reduce symptoms of BPSD?

A

Coping strategies
Antipsychotics
Antidepressants

537
Q

What is the second most common type of dementia?

A

Vascular dementia

538
Q

What is vascular dementia?

A

Dementia caused by reduced blood flow to brain

539
Q

What causes vascular dementia?

A

Subcortical vascular dementia/ small vessel disease (narrowing of small blood vessels in brain)
Stoke (single-infarct dementia)
Multi-infarct dementia (Multiple TIA’s)

540
Q

What are the risk factors for vascular dementia?

A 
Hypertension
Smoking
Poor diet
High cholesterol
Lack of exercise
Obesity
Diabetes
Excess alcohol
Atrial fibrillation
541
Q

What is mixed dementia?

A

Dementia caused by a combination of Alzheimer’s and vascular dementia

542
Q

What are Lewy bodies?

A

Tiny clumps of protein (alpha-synucein)

543
Q

What is Lewy body dementia?

A

Dementia caused by a build up of Lewy bodies in the brain, damaging the way cells work and communicate with each other causing them to die

544
Q

What condition is Lewy body dementia associated with?

A

Parkinson’s disease

545
Q

What is frontotemporal dementia?

A

Dementia caused by abnormal clumping of proteins (e.g. tau) in the frontal and temoral lobes, causin the death of cells and shrinking of the brain

546
Q

What age is frontotemporal dementia usually diagnosed?

A

45-65

547
Q

What are the 3 main symptoms of frontotemporal dementia?

A

Behavioural issues
Progressive aphasia
Semantic dementia (Loss of vocabulary/ understanfing)

548
Q

What is paraplegia and what is the cause?

A

Paralysis of both legs, always caused by spinal cord lesion

549
Q

What is hemiplegia and what is the cause?

A

Paralysis of one side of the body, caused by lesion of the brain

550
Q

What does sensory loss usually indicate?

A

Spinal cord disease

551
Q

What are the three main spinal cord tracts, what do the carry and where to they decussate?

A

Corticospinal: Motor tract that decussates at the medulla
Dorsal colum: Sensory tract (proprioception, vibration, discrimination) that decussates at the medulla
Spinothalamic: Sensory tract (pain, temperature) that decussates in the spinal cord

552
Q

What are upper motor neurone signs?

A

Signs that are contralateral to the lesion, indicating that the lesion is above the anterior horn cell (in the spinal cord, brainstem and motor cortex)

553
Q

What main signs do upper motor neurone lesions cause?

A

Spasticity (increased muscle tone)
Weakness
Hyperreflexia

554
Q

Why does an UMN lesion cause spasticity/ hyperreflexia?

A

Spinal reflex activity is tightly regulated by the brain, and when inhibitory control is lost there is hyperexcitability of the spinal reflexes.

555
Q

What are lower motor neurone signs?

A

Signs that are ipsilateral to the lesion, indicating it is in the anterior horn cell or distal to it

556
Q

What are the signs of a lower motor neurone lesion?

A 
Decreased muscle tone
Atrophy (wasting)
Fasciculations (spontaneous involuntary twitching)
Weakness 
Reduced/ absent reflexes
557
Q

Where is there weakness of in LMN disease?

A

Muscles supplied by involved cord segment, nerve root, part of plexus or peripheral nerve.

558
Q

What is spondylolisthesis?

A

Lower back pain caused by slippage of one vertebra over the one below.

559
Q

What is spondylosis?

A

Degenerative disc disease (type of arthritis)

560
Q

What is myelopathy?

A

Injury to the spinal cord caused by severe compression

561
Q

What is Radiculopathy?

A

Compression of a nerve in the spine.

562
Q

What does myelopathy cause?

A

Upper motor neurone signs: spasticity, weakness, hyperreflexia

563
Q

What does radiculopathy cause?

A

Lower motor neuron signs: decreased tone, wasting, weakness
Pain down dermatome supplied by root
Weakness in myotome supplied by root

564
Q

What are the Myotomes?

A

Group of muscles that a single spinal nerve innervates

565
Q

What are dermatomes?

A

Area of skin that a single nerve innervates

566
Q

What are the dermatomes of the head supplied by?

A

Branches. of the trigeminal nerve

567
Q

What does C5 spinal nerve control?

A 
Shoulder abduction (shrug)
Bicep jerk
568
Q

What does C6 spinal nerve control?

A

Elbow flexion/ supinator jerk

569
Q

What does C7 spinal nerve control?

A

Elbow extension/ tricep jerk

570
Q

What does L3/4 spinal nerve control?

A

Knee extension/ jerk

571
Q

What does L5 spinal nerve control?

A

Ankle dorsiflection (upwards)

572
Q

What does S1 spinal nerve control?

A

Ankle planter flexion (downwards)

573
Q

What does myelopathy (spinal cord compression) cause?

A

Upper neurone signs and symptoms dependent on where the compression is.

574
Q

What is the main cause of spinal cord compression?

A

Vertebral body neoplasms- spinal metastases from breast, prostate and lung cancer

575
Q

What are other common causes of spinal causes?

A

Vertebral body neoplasm
Disc herniation
Disc prolapse

576
Q

What are intervertebral discs?

A

Fibrocartilagenous joint that allows slight movement, ligaments that hold the vertebrae together and acts as a shock absorber to the spine.

577
Q

What is disc herniation?

A

When the centre of the disc (pulposus) moves out through the outer part (annulus), causing pressure on the nerve root and pain

578
Q

What is disc prolapse?

A

When the nucleus pulposus (middle of dic) moves and presses against the annulus but doesn;t escape, producing a bulge in the disc which can put pressure on the nerve root and cause pain.

579
Q

What symptoms does a slipped disc cause? (prolapse or herniation)?

A
  • Lower back pain
  • Numbness
  • Tingling (paraesthesia)
  • Paraplegia
  • Problems bending/ straightening
  • Muscle weakness
  • Sensory loss below level of lesion
580
Q

Which is worse- disc prolapse or herniation?

A

Herniation

581
Q

What are rarer causes of spinal cord compression?

A

Infection
Haematoma
Primary spinal cord tumour

582
Q

What are the red flag signs in spinal cord compression?

A

Loss of bladder/ bowel function
UMN signs in the lower limbs (spasms, hyperreflexia)
LMN signs in upper limbs (atrophy)

583
Q

What investigations can be done to look for spinal cord compression?

A

X-ray whole spine
MRI if indicated
Renal function
Haemoglobin to monitor blood less

584
Q

How is spinal cord compression treated?

A

Dexamethasone until treatment plan confrimed
Catheterisation + Analgesia
Surgical decompression or chemotherapy as indicated.

585
Q

What is sciatica?

A

Compression of the sciatic nerve (usually caused by a herniated disc) at L5/S1, causing pain, numbness and weakness along the sciatic nerve (lower back, buttocks, leg)

586
Q

What is the cauda equina?

A

Sack of nerve roots that extend from the bottom of the spinal cord

587
Q

Where does the spinal cord end?

A

L1-L2

588
Q

What is cauda equine syndrome?

A

When there is compression on the cauda equina

589
Q

What causes cauda equina syndrome?

A 
Spinal damage at or caudal to L1, caused by:
Herniated disc (usually around L5) 
Tumour
Infection
Fracture/ trauma
Spondylolistesis
590
Q

What is the main difference in presentation between cauda equina and lesions higher up the spinal cord?

A

Leg weakness is flaccid and reduced/ absent reflexes (instead of spastic and hyperreflexic)

591
Q

How does cauda equina present?

A 
Bilateral sciatica
Saddle anastesia
Bladder/ bowel dysfunction
Erectile dysfunction
Variable leg weakness (flaccid and areflexic)
592
Q

How is Cauda Equina diagnosed?

A

Rectal exam: loss of anal tone/ sensation
MRI spine
Knee, ankle flexion tests
Straight leg raising, femoral stretch test

593
Q

How is cauda equina treated?

A

Surgical decompression
Immobilise spine
Anti-inflammatories
Chemotherapies if needed

594
Q

What is apraxia?

A

Inability to perform learned/ familiar movement on command, despite willingness to perform the task.

595
Q

What is the action of the precentral gyrus?

A

Primary motor cortex- responsible for executing voluntary movements

596
Q

What are the steps in the organisation of movement?

A
  1. Idea of movement (in various areas of cortec)
  2. Activation of upper motor neurones in pre central gyrus
  3. Impulses travel to lower motor neurones via corticospinal tract
  4. Cerebellum and basal ganglia modulate activity
597
Q

What is a motor unit?

A

The basic functional unit of muscle activity: an alpha motor neurone (LMN) + axon + the skeletal fibres it innervates

598
Q

What regulates muscle tone?

A

Stretch receptors in muscle (muscle spindles) innervated by gamma motor neurones.
Regulated by local spinal cord reflexes

599
Q

What is muscle tone?

A

The maintenance of partial contraction of a muscle, important for generating reflexes, maintaining posture and balance, and controlling proper function of other organ systems.

600
Q

What are the potential sites of damage along the motor pathway?

A 
Motor nuclei of cranial nerves
Motor neurones in spinal cord
Spinal ventral roots
Peripheral nerves
Neuromuscular junction
Muscle
601
Q

What are upper motor neurone signs?

A 
Everything goes up!:
Spasticity (increased muscle tone)
Brisk reflexes
Plantars upturned on stimulation
Limb muscle weakness in characteristic pattern
602
Q

What is a positive Babinski sign?

A

Plantars upturned on stimulation

603
Q

What is the characteristic limb muscle weakness in upper motor neurone disease?

A

Upper limb extensors weaker than flexors
Lower limb flexors weaker than extensors
Impaired finer movement

604
Q

What are lower motor neurone signs?

A 
Everything goes down!:
Flaccid (reduced muscle tone)
Muscle wasting
Fasciculation (spontaneous contractions)
Depressed/ absent reflexes
605
Q

What are the 6 mechanisms that can cause nerve malfunction?

A 
Demyelination
Axonal degeneration
Compression
Infarction
Infiltration
Wallerian degeneration
606
Q

What does demyelination cause and what is an example?

A

Marked slowing of conduction (e.g. Guillain-Barre syndrome)

607
Q

What is Wallerian degeneration?

A

Process that results when a nerve fibre is cut or crushed, and the part of the axon distal to the injury degenerates.

608
Q

What are the different types of peripheral nerve disease?

A

Neuropathy
Mononeuropathy
Mononeuritis multiplex
Polyneuropathy

609
Q

What is mononeuritis multiplex?

A

When 2 or more individual nerves are affected

610
Q

What is a polyneuropathy?

A

When many nerves in different parts of the body are involved (can be sensory, motor or both)

611
Q

What is the usually cause of a mononeuropathy?

A

Local cause: trauma or entrapment (e.g. tumour)

612
Q

What are the causes of mononeuritis multiplex?

A 
Wegener's granulmatosis
Aids/ Amyloid
Rheumatoid arthritis
Diabetes mellitus
Sarcoidosis
Polyarteritis nodosa
Leprosy
Carcinoma
613
Q

What is the most common mononeuropathy?

A

Carpal tunnel syndrome

614
Q

What happens incarpal tunnel syndrome?

A

Pressure and compression. onthe median nerve as it passes through the carpal tunnel in the wrist.

615
Q

What is the cause of carpal tunnel syndrome?

A

Idiopathic

Associated with hypothyroidism, diabetes, pregnancy, amyloidosis, obesity, RA and acromegaly

616
Q

What are the symptoms of carpal tunnel syndrome?

A

Ache in fingers, hand or arm (worse at night)
Numb hands
Tingling/ pins and needles (Paraesthesiae)
Weak thumb
(symptoms are intermittent and progressive)

617
Q

How can carpal tunnel syndrome be managed?

A

Wrist splint (relieves pressure on nerve)
Stop things that trigger it (e.g. vibrating work tools, playing an instrument)
Painkillers
Surgery

618
Q

Where does the median nerve arise and what is its main action?

A

C6-T1 (Brachial plexus)

Precision grip

619
Q

What muscles are innervated by the median nerve?

A 
LOAF:
2 Lumbricals
Opponens pollicis
Abductor pollicis brevis
Flexor pollicis brevis
620
Q

Where does the ulnar nerve arise and what is its main actions?

A

C7-T1 (Brachial plexus)

Responsible for flexing at the elbow

621
Q

Where does the radial nerve arise and what is its main actions?

A

C5-T1

Opening the fist

622
Q

What are the most common nerve mononeuropathies?

A 
Median
Ulnar
Radial
Sciatic
Tibial
Phrenic
Peroneal
623
Q

What are the 3 categories of peripheral nerve injuries?

A

Stretch related, lacerations, compressions

624
Q

How can polyneuropathies be classified?

A 
By course (acute or chronic)
By function (sensory, motor, autonomic or mixed)
By pathology (demyelination, axonal degeneration, both)
625
Q

What are the causes of polyneuropathies?

A 
Metabolic
Vasculitides
Malignancy
Inflammatory
Infections
Nutritional (deficiencies)
Inherited syndromes
Drugs/ toxins
626
Q

What are the metabolic causes of polyneuropathy?

A

Diabetes
Renal failure
Hypothyroidism
Hypoglycaemia

627
Q

What is the clinical presentation of a sensory polyneuropathy?

A

Numbness
Pins & needles
Glove and stocking distribution

628
Q

What are the clinical presentations of a motor neuropathy?

A 
Often progressive
Weak/ clumsy
Difficult walking or breathing
Wasting/ 
Reduced/ absent reflexes
629
Q

Where are the cranial nerve nuclei located?

A

Brainstem (medulla, pons and midbrain)

630
Q

What can cause cranial nerve lesions?

A 
Brainstem problems: 
Tumour
MS
Trauma
Aneurysm
Vertebral artery dissection (infarction)
Infection
631
Q

What happens in a CN3 palsy?

A

Oculomotor:
Ptosis (drooping eyelid)
Fixed dilated pupil
Eye down and out

632
Q

What happens in a CN4 palsy?

A

Trochlear nerve:

Innervates superior oblique so results in a head tilt to correct extortion

633
Q

What happens in a CN6 palsy?

A

Abducens:

Innervates the lateral rectus eye muscle so eye is adducted

634
Q

What happens in a CN5 palsy?

A

Trigeminal nerve:
Jaw deviation
Loss of corneal reflex

635
Q

What happens in a CN7 palsy?

A

Facial nerve:

Facial droop and weakness

636
Q

What happens in a CN8 palsy?

A

Vestibulocochlear nerve:
Hearing impairment
Vertigo/ lack of balance

637
Q

What happens in a CN9/10 palsy?

A

Glossopharyngeal/ vagus:
Gag reflex and swallowing issues
Vocal issues

638
Q

What is autonomic neuropathy?

A

Damage to the nerves that control involuntary bodily processes (e.g. digestion, bladder function, blood pressure)

639
Q

How might autonomic neuropathy present?

A 
Postural hypotension (faint on standing)
Ejaculator failure
Reduced sweating
Erectile dysfunction
Constipation
Nocturnal diarrhoea
Urine retention
640
Q

What is the Purkinje layer of the cerebellum?

A

The outer layer, that is the only area of output.

641
Q

What is syncope?

A

Temporary loss of consciousness due to disruption of blood flow to the brain

642
Q

What causes a vasovagal episode (fainting)?

A

Problem with the autonomic system regulating blood flow to the brain: When the vagus nerve receives a strong stimulus (e.g. emotional event, change in temperature), it can stimulate the parasympathetic nervous system. This dilates the vessels in the brain, reducing the pressure in the cerebral circulation and leading to hypoperfusion.

643
Q

What is the prodome?

A

The feeling prior to fainting which may involve feeling:

  • Hot/ clammy
  • Sweaty
  • Heavy
  • Dizzy/ lightheaded
  • Dark/ blurry vision
  • Headache

PHASE 2A (Mine) (15 decks)

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