Rachael Penn Flashcards

1
Q

Visual field pathway

A

optic lens to temporal retina, to optic nerve to optic chiasm, down optic tract to lateral geniculate nucleus to the primary visual cortex

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2
Q

describe the afferent pupillary reflex

A

light is shone in one eye, travels down the efferent pathway to the pretectal nucleus, then back to the iris sphincter muscle via the afferent pathway

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3
Q

how does quadrantanopia occur

A

2 tracts to the occipital cortex- an upper and lower one, hence you get quadrantanopia

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4
Q

how do you establish visual acuity?

A
  • Stand the patient at 6 metres from the Snellen chart.
  • Ask the patient to cover one eye and read the lowest line they are able to.
  • Record the lowest line the patient was able to read (e.g. 6/6 (metric) which is equivalent to 20/20 (imperial)).
  • You can have the patient read through a pinhole to see if this improves vision (if vision is improved with a pinhole, it suggests there is a refractive component to the patient’s poor vision).
  • Repeat the above steps with the other eye.
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5
Q

what are dawson’s fingers?

A

Dawson fingers are a radiographic feature of demyelination characterised by periventricular demyelinating plaques distributed along the axis of medullary veins, perpendicular to the body of the lateral ventricles and/or callosal junction.
This is thought to reflect perivenular inflammation.
They are a relatively specific sign for multiple sclerosis.

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6
Q

how is an AP propagated down an axon?

A

Neurotransmitters will bind to receptors on the dendrites of the neuron, and cause opening of the voltage gated ion channels. There is influx of positive ions (Na) into the neuron (normally a cell is negative inside and positive outside), causing depolarisation of the membrane. When the depolarisation threshold has been reached, sodium channels in the hillock of the neuron open, initiating an action potential. The neuron completely depolarises and once depolarisation is completed, the Na channels close and VGKC open allowing potassium out of the cell, allowing repolarisation back to the resting state.

Nodes of Ranvier are natural gaps in the myelin sheath, which serve to speed up the rate of conduction. The action potential will jump in saltatory conduction which allow the potential to be propagated.

The speed of conduction is influenced by axon diameter and axon resistance to current leak. Myelin acts as an insulator that prevents the current leaving the axon, thus increasing the speed of conduction.

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7
Q

what is a visual evoked potential

A

Used to assess the optic nerve pathway
Measures the speed of nerve conduction along sensory nerves to the brain- sometimes used in MS diagnosis.
Patient is shown a flashing chessboard pattern and electrodes are placed on the scalp to monitor brain activity in response to the visual signals. This is repeated for each eye

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8
Q

flow of CSF

A

produced by choroid plexus in lateral ventricle

exits via foramen of Monro to the 3rd ventricle. more CSF added

to the 4th ventricle via the cerebral aqueduct. more CSF added

CSf flows out of the foramen of Magendie (medial) and the foramen of Lushka (lateral) into the subarach space

absorbed by the arachnoid villi in the venous sinuses

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9
Q

analysis of CSF in a petient with suspected MS

A

Cerebral spinal fluid studies can confirm demyelinating disease of the nervous system.

They show an increase in immunoglobulin concentrations in more than 90% of patients with MS.

IgG index (a comparison between IgG levels in the CSF and in the serum) is elevated in many MS patients- >0.66 indicative of MS

Oligoclonal Immunoglobulin Bands can be identified in the CSF of MS patients via electrophoresis.

The overall protein level is also slightly elevated - up to 0.1 g/L. Protein level can be higher if the patient is going through a marked relapse (i.e.,. severe optic neuritis)- released by the demyelination process.

Some patients also exhibit a slight elevation in cell count (up to 50 per cubic millimeter )- most cells can be identified as T-lymphocytes.

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10
Q

why take a blood test and CSF sample?

A

If proteins are found in the CSF but not in the blood, it is indicative of an MS diagnosis.

Also helps to screen for other abnormalities

Also to measure glucose levels- should be comparable between blood and CSF

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11
Q

what criteria are used to diagnose MS

A

McDonald criteria

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12
Q

LEARN MCDONALD CRITERIA

A

https://mstrust.org.uk/a-z/mcdonald-criteria

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13
Q

review the corticospinal tract

A

Begin in the cerebral cortex and receive input from primary motor cortex, premotor cortex, supplementary motor area and somatosensory area.

Originate in the cortex, neurones then come together and descend through the internal capsule (white matter pathway between the thalamus and basal ganglia) clinical importance: internal capsule is susceptible to compression e.g. haemorrhagic bleeds which could cause lesions of the descending tracts.

Neurons then pass through the crus cerebri of the midbrain, then through the pons and the medulla.

The tract then divides into two at the inferior part of the medulla: the fibres in the lateral corticospinal tract cross over (decussate) and then descend in the spinal cord, terminating at the ventral horn at each segmental level. From the ventral horn, the neurons synapse onto lower motor neurons and supply the muscles of the body.

The anterior corticospinal tract does not decussate at the medulla and descends in the spinal cord. At the ventral horn of the cervical and upper thoracic segmental levels, the tract decussates and terminates.

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14
Q
  1. Outline the natural history of MS (Benign, remitting and relapsing, primary progressive and secondary progressive MS)
A

Benign MS
• A type of relapsing and remitting MS with mild or no attacks separated by long periods of no symptoms
• Can only be benign MS if the patient has been 15 years relapse and symptom free with little or no disability
• It is still possible to relapse even if MS has been benign

Remitting and relapsing MS
• People have attacks of new and old symptoms
• ~85% patients with MS have this type
• Relapse is defined as “the appearance of new symptoms, or the return of old symptoms, for a period of 24hours or more- in the absence of a change in core body temperature or infection”
• Triggers vary person to person, but some common ones include
o Stress
o Infection
o Vaccination
o Pregnancy- in the few months after delivery

Primary progressive
• Affects about 10-15% people
• Progressive disease from onset of first symptoms
• Symptoms get worse over time rather than appearing as sudden relapses
• Early symptoms are often subtle such as walking problems
• Although symptoms get progressively worse, there are periods of time when they can be stable
• Usually diagnosed in patients in their 40-50s
• Can also get progressive relapsing MS: progressive MS as well as relapses- now being called active progressive MS

Secondary progressive
• A stage of MS which typically comes after relapsing-remitting MS
• Disability gradually worsens
• No longer likely to get relapses
• Fewer people are developing this due to DMTs

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15
Q

complications of MS

A
  • Muscle stiffness or spasm
  • Paralysis, typically in the legs
  • Problems with bladder, bowel, or sexual function
  • Mental changes such as forgetfulness or mood swings
  • Depression- sleep disturbance can contribute
  • Epilepsy
  • Chest or bladder infections
  • Swallowing difficulties
  • Osteopenia and osteoporosis
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16
Q

tx for MS relapse

A

steroids

methylprednisolone

17
Q

symptomatic treatments for specific problems

A
  • painkillers e.g. paracetamol and gabapentin
  • physiotherapy
  • CBT for anxiety and depression
  • Rehabilitation to improve day to day living
  • Exercise e.g. Tai Chi, Pilates, yoga
  • Meditation and mindfulness
  • Have to pay for prescriptions
  • GABA agonists for spasticity
  • Beta blockers for tremor
  • Anti-convulsant for painful paraesthesia e.g. carbamazepine
18
Q

MDT in MS

A
  • Physio
  • OT
  • Social worker
  • SALT
  • Counsellor
  • MS nurse- can also request for a neurology nurse if an MS nurse isn’t available
  • Neurologist
  • Continence advisor
  • Dietician
  • Psychologist/neuropsychologist
  • Rehabilitation team
  • Pharmacist
  • Urologist
19
Q

clinical signs of upper motor motor lesion

A
  • Weakness
  • Spasticity
  • Clonus- involuntary muscle contractions
  • Hyperreflexia- reflexes are due to lower motor neurons, normally UMN modulate it- when there is a lesion there is no modulation hence hyperreflexia- loss of inhibition.
  • Babinsky reflex positive- stroke the bottom of the foot, big toe will pull back and other toes will spread out, should disappear at 2 years of age
  • Cortical sensations
20
Q

what are upper motor functions

A

Responsible for the coordination of movement. The major UMN tract is the pyramidal tract which divides into the corticospinal and corticobulbar tracts. Lesion above the medulla (where the fibres cross over) results in contralateral symptoms, below the medullary pyramids= ipsilateral symptoms. Corticobulbar tract doesn’t cross ove

21
Q

clinical symptoms of lower motor neurone lesion

A
  • Muscle atrophy
  • Fasciculations (muscle twitching)
  • Decreased reflexes
  • Reduced tone
  • Negative Babinsky sign
  • Flaccid paralysis
  • Absent tendon reflexes
22
Q

symptoms of cerebellar lesions

A

DANISH
• Dysdiadochokinesia- difficulty carrying out rapid, alternating movements
• Ataxia
• Nystagmus
• Intention tremor- tremor gets worse as it approaches an object it was aiming for
• Scanning speech- spoken word is broken up into separate syllables
• Hypotonia

23
Q

MICA oxybutynin

A
  • MOA: antispasmodic actions on the bladder, relieving the symptoms of an overactive bladder. Inhibits muscarinic action of Ach on the smooth muscle, but not skeletal muscle. The active metabolite competitively inhibits the postganglionic type 1, 2, and 3 muscarinic receptors. Leads to increased urine capacity in the bladder, decreased urgency and frequency. Delays the initial desire to void.
  • Indications: urinary frequency, urinary urgency, urinary incontinence, neurogenic bladder instability, nocturnal enuresis (bed wetting) associated with overactive bladder
  • Contraindications: angle-closure glaucoma, GI obstruction, intestinal atony, MG, paralytic ileus, pyloric stenosis, severe UC, significant bladder outflow obstruction, toxic megacolon, urinary retention. Avoid in pregnancy and breast feeding.
  • Adverse effects: constipation, diarrhoea, dizziness, drowsiness, dry mouth, dyspepsia, flushing, headache, nausea, palpitations, skin reactions, tachycardia, urinary disorders, vision disorders, vomiting
24
Q

MICA tolterodine

A
  • MOA: competitive antagonist of muscarinic receptors (M2 and M3). Causes inhibition of bladder contraction, decrease in detrusor pressure and decreased incomplete emptying of bladder.
  • Indications: urinary frequency, urgency, incontinence
  • Contraindications: same as oxybutynin and history of QT interval prolongation
  • Adverse effects: abdominal pain, bronchitis, chest pain, diarrhoea, dry eye, fatigue, GI disorders, paraesthesia, peripheral oedema, vertigo, weight increased, arrhythmia, heart failure, memory loss, weight increased, arrhythmia, heart failure, memory loss, nervousness, hallucination.
25
Q

what is charcots triad for neuro

A
  • Nystagmus
  • Intention tremor
  • Scanning or staccato speech