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P3A Med > Neurology > Flashcards

Neurology Flashcards

1
Q

Describe the pathophysiology behind Alzheimer’s Disease.

A

A progressive degeneration of the cerebral cortex. Neurons affected develop surrounding amyloid plaques, neurofibrillary tangles, and produce less acetylcholine.

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2
Q

How is Alzheimer’s Disease treated pharmacologically?

A

AChE inhibitors appear to be beneficial for people with mild to moderate Alzheimer’s disease.

Memantine is cost-effective in the management of moderate and severe Alzheimer’s disease

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3
Q

Give example AChE inhibitors

A

Donepezil, galantamine, rivastigmine

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4
Q

How do AChE inhibitors work?

A

Anticholinesterases are a class of drugs that decrease breakdown of acetylcholine (a chemical messenger in the brain) and can be used in conditions whereby there is an apparent lack of this messenger transmission such as in Alzheimer’s disease.

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5
Q

How is narcolepsy treated pharmacologically?

A

First-line is modafinil (but note subsequent MHRA warnings).

Second-line is methylphenidate.

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6
Q

What is modafinil? When can it not be used?

A

Treats excessive daytime sleepiness, multiple contra-indications

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7
Q

What is methylphenidate?

A

A stimulant - has many side effects

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8
Q

How is cataplexy treated pharmacologically?

A

Sodium oxybate (first line), and/or antidepressants

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9
Q

Why do we avoid tricyclics in Alzheimer’s care?

A

Because they, and anticholinergics, can worsen cognitive decline

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10
Q

Describe the triad of Wernicke’s encephalopathy

A

Ophthalmoplegia, global confusion, gait ataxia

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11
Q

What is Korsakoff Syndrome?

A

Wernicke’s enceph + amnesia leading to confabulation

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12
Q

Describe the pathophysiology behind Korsakoff Syndrome

A

The mamillary bodies are affected in the limbic system, so pts confabulate stories to fill in the gaps

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13
Q

How do we treat Wernicke’s encephalopathy?

A

Wernicke’s encephalopathy is a medical emergency. Thiamine orally (IM or IV may be used in secondary care) plus vitamin B complex or multivitamins.

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14
Q

LMN vs. UMN: Where would you find disuse atrophy?

A

UMN: if you don’t use it you lose it (can’t willingly activate muscle). Loss of 15-20%.

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15
Q

LMN vs. UMN: Where would you find denervation atrophy?

A

LMN: lack of LMN stimulation leads to reduced ACh secretion. This reduces muscle contraction, and reduces activation of an intracellular pathway that produces TFs, which would increase protein synthesis. The decreased protein synthesis leads to increased proteolysis, so the muscle breaks down. Loss of up to 70-80%.

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16
Q

What are fasciculations?

A

Pathological muscle contraction seen with LMN lesions, similar to a muscle twitch

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17
Q

Describe the pathophysiology behind fasciculations

A

Reduced ACh in the synaptic cleft leads to decreased activity of ACh receptors on the muscle, which leads to upregulation of the ACh receptors (more are made). This shifts the resting potential closer to the threshold potential, so it is easier to mechanically activate the chemically-gated ACh receptors, leading to pathological muscle contraction.

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18
Q

What are fibrillations?

A

Fasciculations but seen on an EMG

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19
Q

Why is there hypertonia in UMN lesion?

A

The medullary reticulospinal nuclei aren’t triggered, so the LMN isn’t inhibited, and there is increased alpha motor neuron activity to the extrafusal fibres - increasing their tone.

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20
Q

Why is there hyperreflexia in UMN lesion?

A

The medullary reticulospinal nuclei aren’t triggered, so the LMN isn’t inhibited, and there is increased gamma motor neuron activity to the intrafusal fibres - increasing the sensitivity of the muscle spindles, leading to hyperreflexia.

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21
Q

What is spastic paralysis?

A

Loss of muscle strength due to the combined effects of hypertonia and hyperreflexia in UMN lesion

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22
Q

What is the difference between spasticity and rigidity?

A

Spasticity is velocity dependant - it increases with speed - and is unidirectional. Rigidity is velocity independent, and is bidirectional.

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23
Q

What is the clasp-knife phenomenon?

A

Clasp-knife response refers to a Golgi tendon reflex with a rapid decrease in resistance when attempting to flex a joint. Seen in UMN lesion.

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24
Q

What is flaccid paralysis?

A

Loss of muscle strength due to hypotonia and hyporeflexia - seen in LMN lesion

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25
Q

Why do you see the Babinski reflex with UMN lesions?

A

The corticospinal tract inhibits the reflex causing dorsiflexion of the foot. When this inhibition is no longer present, this reflex is hyperreactive. They become so hyperreactive that the dorsiflexors overcome the plantar-flexors, and the foot then dorsiflexes instead of plantar-flexes.

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26
Q

Where do you see Babinski reflexes other than with UMN lesions?

A

In children typically less than one year old. The corticospinal tract should be heavily myelinated, but this myelination is developing in v. young children.

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27
Q

What is Hoffman’s sign?

A

The Hoffman sign is an involuntary flexion movement of the thumb and or index finger when the examiner flicks the fingernail of the middle finger down.

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28
Q

Where do you see pronator drift?

A

UMN lesion

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29
Q

What is neurofibromatosis?

A

A genetic condition that causes nerve tumours (neuromas) to develop throughout the nervous system. These tumours are benign, however they do cause neurological and structural problems

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30
Q

What is the NF1 gene?

A

The neurofibromatosis type 1 gene is found on chromosome 17. It codes for a protein called neurofibromin, which is a tumour suppressor protein.

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31
Q

How do we diagnose type one neurofibromatosis?

A

CRABBING, 2 of the following 7: Cafe-au-lait spots (6 or more), relative with NF1, axillary or inguinal freckles, bony dysplasia such as bowing of a long bone or sphenoid wing dysplasia, iris hamartomas (Lisch nodules) (2 or more) are yellow brown spots on the iris, neurofibromas (2 or more) or 1 plexiform neurofibroma, glioma of the optic nerve. Good luck.

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32
Q

How do we treat neurofibromatosis?

A

Management of symptoms, not direct treatment

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33
Q

Where do you see bilateral acoustic neuromas?

A

Type 2 neurofibromatosis. Acoustic neuromas lead to hearing loss, tinnitus and balance problems.

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34
Q

What pattern of inheritance does NF1 show?

A

Inheritance of mutations in this gene is autosomal dominant

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35
Q

What is motor neurone disease?

A

Motor neurone disease is a progressive, ultimately fatal condition where the motor neurones stop functioning. There is no effect on the sensory neurones and patients should not experience any sensory symptoms.

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36
Q

Describe the pathophysiology of MND

A

Mechanism not understood. There is progressive degeneration of both upper and lower motor neurones. The sensory neurones are spared.

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37
Q

What is dysarthria?

A

Slurred speech

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38
Q

How is MND treated?

A

Best tx is riluzole at the moment. Slows progression of the disease. Can extend life by a few months in AML.

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39
Q

How does MND present?

A

The typical patient is a late middle aged man, possibly with an affected relative. There is an insidious, progressive weakness of the muscles throughout the body affecting the limbs, trunk, face and speech. The weakness is often first noticed in the upper limbs. There may be increased fatigue when exercising. They may complain of clumsiness, dropping things more often or tripping over. They can develop slurred speech (dysarthria). UMN & LMN signs.

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40
Q

What is multiple sclerosis?

A

A chronic and progressive condition that involves demyelination of the myelinated neurones in the central nervous system

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41
Q

Describe the epidemiology of MS.

A

MS typically presents in young adults (under 50 years) and is more common women. Symptoms tend to improve in pregnancy and in the postpartum period.

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42
Q

Describe the pathophysiology of MS.

A

Oligodendrocytes create myelin in the CNS (Schwann cells = PNS). There is inflammation around myelin in the CNS and infiltration of immune cells that cause damage to the myelin.

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43
Q

How is MS diagnosed?

A

MRI: multiple lesions disseminated in time and space”

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44
Q

Give four causes of MS.

A

Epstein-Barr Virus, genetics, low VitD, smoking, obesity

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45
Q

How does MS present?

A

Optic neuritis, eye movement abnormalities, focal weakness, focal sensory symptoms, ataxia

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46
Q

Describe the eye movement abnormalities sometimes seen in MS.

A

Unilateral lesions in the sixth nerve causes a condition called internuclear ophthalmoplegia. Internuclear refers to the nerve fibres that connect between the cranial nerve nuclei that control eye movements (3rd, 4th and 6th cranial nerve nuclei). The internuclear nerve fibres are responsible for coordinating the eye movements to ensure the eyes move together. Ophthalmoplegia means a problem with the muscles around the eye.

Lesions in the sixth cranial nerve cause a conjugate lateral gaze disorder. Conjugate means connected. Lateral gaze is where both eyes move together to look laterally to the left or right. It is disordered in a sixth cranial nerve palsy. When looking laterally in the direction of the affected eye, the affected eye will not be able to abduct. For example, in a lesion affecting the left eye, when looking to the left, the right eye will adduct (move towards the nose) and the left eye will remain in the middle as the muscle responsible for making it move laterally is not functioning.

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47
Q

If a patient with MS had a LP, what might you see in the CSF?

A

Oligoclonal bands

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48
Q

How does optic neuritis present?

A

Central scotoma. This is an enlarged blind spot.
Pain on eye movement
Impaired colour vision
Relative afferent pupillary defect

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49
Q

How do we treat relapses of MS?

A

Relapses can be treated with steroids. NICE recommend methylprednisolone.

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50
Q

How do we treat spasticity?

A

Baclofen, gabapentin and/or physiotherapy

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51
Q

How do we treat urge incontinence pharmacologically?

A

Anticholinergic medications such as tolterodine or oxybutynin

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52
Q

How can we treat neuropathic pain pharmacologically?

A

Amitriptyline or gabapentin

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53
Q

What is hydrocephalus?

A

Cerebrospinal fluid (CSF) building up abnormally within the brain and spinal cord. This is a result of either over-production of CSF or a problem with draining or absorbing CSF.

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54
Q

Describe the physiology of the production of CSF.

A

CSF is created in the four choroid plexuses (one in each ventricle) and by the walls of the ventricles. CSF is absorbed into the venous system by the arachnoid granulations.

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55
Q

What is the most common cause of hydrocephalus? Describe its pathophysiology.

A

Aqueductal stenosis, leading to insufficiency drainage of CSF. The cerebral aqueduct that connects the third and fourth ventricle is stenosed (narrowed). This blocks the normal flow of CSF out of the fourth ventricle, causing CSF to build up in the lateral and third ventricles.

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56
Q

How does hydrocephalus present in children?

A

The cranial bones in babies are not fused at the sutures until around 2 years of age. Therefore, the skull is able to expand to fit the cranial contents. When a baby has hydrocephalus it causes outward pressure on the cranial bones. Therefore, babies with hydrocephalus will have an enlarged and rapidly increasing head circumference (occipitofrontal circumference).

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57
Q

How is hydrocephalus treated?

A

Placing a VP shunt that drains CSF from the ventricles into another body cavity is the mainstay of treatment for hydrocephalus. Usually the peritoneal cavity is used to drain CSF, as there is plenty of space and it is easily reabsorbed. Typically need replacing in children after 2 years.

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58
Q

What is normal pressure hydrocephalus?

A

The condition of ventricular dilatation in the absence of raised CSF pressure on lumbar puncture

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59
Q

How does normal pressure hydrocephalus present?

A

A triad of gait abnormality, urinary (usually) incontinence and dementia

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60
Q

Describe the epidemiology of NPH.

A

The condition occurs mainly in elderly patients, increasing in prevalence with age

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61
Q

Why do you find gait abnormalities in NPH?

A

Due to distortion of the corona radiata by the dilated ventricles. This area contains the sacral motor fibres than innervate the legs

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62
Q

Why do you find urinary incontinence in NPH?

A

Due to involvement of the sacral nerve supply that innervates the sphincter

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63
Q

Why do you see dementia in NPH?

A

Due to distortion of the periventricular limbic system. Slower onset than AD.

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64
Q

Give causes of increased intracranial pressure.

A

Malignancy, haematoma, abscess, oedema, venous obstruction, idiopathic

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65
Q

How does raised ICP present?

A

Headache, swollen optic disc, vomiting, mental state changes,

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66
Q

How do we investigate raised ICP?

A

CT/MRI to determine if there’s any underlying lesions, BCG, renal function, U&E, FBC

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67
Q

What are the priorities when treated raised ICP in the emergency setting?

A

In the acute emergency situation the priority is maintaining adequate arterial oxygen tension and ensuring normal vascular volume and normal osmosis. It is also essential to maintain normoglycaemia. Otherwise treatment depends on cause.

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68
Q

Give tx for raised ICP in the emergency setting.

A

Avoid pyrexia (raises ICP), manage seizures, CSF drainage, elevate head of bed, analgesia,

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69
Q

Give the five branches of the facial nerve

A

Temporal, zygomatic, buccal, marginal mandibular, cervical

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70
Q

What are the three functions of the facial nerve?

A

Motor: Supplies the muscles of facial expression, the stapedius in the inner ear and the posterior digastric, stylohyoid and platysma muscles in the neck.

Sensory: carries taste from the anterior 2/3 of the tongue.

Parasympathetic: it provides the parasympathetic supply to the submandibular and sublingual salivary glands and the lacrimal gland (stimulating tear production).

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71
Q

How do you distinguish between UMN and LMN facial lesion?

A

Each side of the forehead has upper motor neurone innervation by both sides of the brain. Each side of the forehead only has lower motor neurone innervation from one side of the brain.

In an upper motor neurone lesion, the forehead will be spared and the patient can move their forehead on the affected side.

In a lower motor neurone lesion, the forehead will NOT be spared and the patient cannot move their forehead on the affected side.

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72
Q

What is Bell’s Palsy?

A

An idiopathic condition presenting as a unilateral lower motor neurone facial nerve palsy. Recovery takes from several weeks to a year

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73
Q

How do we treat Bell’s Palsy?

A

If they present within 72hrs of symptom onset, treat with prednisolone. Patients also require lubricating eye drops to prevent the eye on the affected drying out and being damaged.

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74
Q

What is Ramsay-Hunt syndrome?

A

Caused by the herpes zoster virus, it presents as a unilateral lower motor neurone facial nerve palsy.

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75
Q

Give symptoms/signs of RH syndrome.

A

Patients stereotypically have a painful and tender vesicular rash in the ear canal, pinna and around the ear on the affected side. This rash can extend to the anterior 2/3 of the tongue and hard palate.

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76
Q

How is RH syndrome treated?

A

Prednisolone and acyclovir, lubricating eye drops

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77
Q

What causes the non-blanching petechial rash in meningitis?

A

Meningococcal septicaemia is the cause of the classic “non-blanching rash” that everybody worries about as it indicates the infection has caused disseminated intravascular coagulopathy (DIC) and subcutaneous haemorrhages.

78
Q

Name the two most common causes of bacterial meningitis

A

Neisseria meningitidis (meningococcus) and Streptococcus pneumoniae (pneumococcus)

79
Q

How does meningitis present in very young children and neonates?

A

Very non-specific signs and symptoms such as hypotonia, poor feeding, lethargy, hypothermia and a bulging fontanelle.

80
Q

How do you diagnose meningitis in neonates or very young children?

A

LP: In all children which are…
Under 1 m.o. presenting with fever
1 – 3 m.o. with fever and are unwell
Under 1 y.o. with unexplained fever and other features of serious illness

81
Q

What is Kernig’s test?

A

This involves lying the patient on their back, flexing one hip and knee to 90 degrees and then slowly straightening the knee whilst keeping the hip flexed at 90 degrees. This creates a slight stretch in the meninges and where there is meningitis will produce spinal pain or resistance to this movement.

82
Q

What is Brudzinski’s test?

A

Brudzinski’s test involves lying the patient flat on their back and gently using your hands to lift their head and neck off the bed and flex their chin to their chest. A positive test is when this causes the patient to involuntarily flex their hips and knees.

83
Q

How is meningitis treated in the community?

A

IM Benzylpenicillin + transfer to hospital

84
Q

How is meningitis treated in secondary care?

A

< 3 months – cefotaxime plus amoxicillin (the amoxicillin is to cover listeria contracted during pregnancy from the mother)

> 3 months – ceftriaxone

Vancomycin should be added to these if there is a risk of penicillin resistant pneumococcal infection such as from recent foreign travel or prolonged antibiotic exposure.

Steroids are also used in bacterial meningitis to reduce the frequency and severity of hearing loss and neurological damage. Dexamethasone is given 4 times daily for 4 days to children over 3 months if the lumbar puncture is suggestive of bacterial meningitis.

85
Q

Why do we contact close contacts of meningitis pts?

A

So we can give post exposure prophylaxis. The usual antibiotic choice for this is a single dose of ciprofloxacin. It should be given as soon as possible and ideally within 24 hours of the initial diagnosis.

86
Q

What are the most common causes of viral meningitis?

A

Herpes simplex virus (HSV), enterovirus and varicella zoster virus (VZV). A sample of the CSF from the lumbar puncture should be sent for viral PCR testing.

87
Q

What is Horner’s syndrome?

A

A rare condition that results from disruption of the sympathetic nerves supplying the eye

88
Q

What is the Horner’s triad?

A 
Partial ptosis (upper eyelid drooping).
Miosis (pupillary constriction) leading to anisocoria (difference in size of the pupils).
Hemifacial anhidrosis (absence of sweating).
89
Q

Give three causes of Horner’s syndrome.

A

CNS lesions, apical lung tumours, herpes zoster infection

90
Q

What is cerebral palsy?

A

A highly variable disease characterised by permanent neurological problems resulting from damage to the brain around the time of birth. It is not a progressive condition, however the nature of the symptoms and problems may change over time during growth and development

91
Q

List five causes of cerebral palsy.

A

Maternal infections, trauma during pregnancy, birth asphyxia, pre-term birth, meningitis, severe neonatal jaundice, head injury

92
Q

What are the three main types of cerebral palsy?

A

Spastic, dyskinetic, ataxic

93
Q

What is spastic cerebral palsy?

A

Hypertonia (increased tone) and reduced function resulting from damage to upper motor neurones

94
Q

What is dyskinetic cerebral palsy?

A

Problems controlling muscle tone, with hypertonia and hypotonia, causing athetoid movements and oro-motor problems. This is the result of damage to the basal ganglia.

95
Q

What is ataxic cerebral palsy?

A

Problems with coordinated movement resulting from damage to the cerebellum

96
Q

What is hemiplegia?

A

Where one side of the body is affected

97
Q

What is diplegia?

A

Where all four limbs are affected, but mostly the legs

98
Q

What is quadriplegia?

A

Where all four limbs are affected more severely, often with seizures, speech disturbance and other impairments

99
Q

How does cerebral palsy present in childhood?

A

Failure to meet milestones, increased/decreased tone, hand preference below 18 months (LEARN THIS), problems with coordination, sensation or walking; feeding or swallowing problems, learning difficulties

100
Q

What does hemiplegic/diplegic gait show?

A

Indicates an upper motor neuron lesion

101
Q

What does broad-based/ataxic gait show?

A

A cerebellar lesion

102
Q

What does high-stepping gait show?

A

Foot drop or LMN lesion

103
Q

What does waddling gait show?

A

Indicates pelvic muscle weakness due to myopathy

104
Q

What is an antalgic gait?

A

A limp, indicates localised pain

105
Q

A patient with cerebral palsy comes to see you in the clinic. You ask to see their gait. What might it show?

A

Hemiplegic or diplegic gait. This gait is caused by increased muscle tone and spasticity in the legs. The leg will be extended with plantar flexion of the feet and toes. This means they have to swing the leg around in a large semicircle when moving their leg from behind them to in front. There is not enough space to swing the extended leg in a straight line below them.

106
Q

What is the differential diagnosis of UMN lesion?

A

Acquired brain injury or tumour.

107
Q

What is baclofen?

A

A muscle relaxant

108
Q

What do we use glycopyrronium bromide for?

A

Excessive drooling

109
Q

What is myasthenia gravis?

A

An autoimmune condition that causes muscle weakness that gets progressively worse with activity and improves with rest

110
Q

Describe the epidemiology of myasthenia gravis.

A

Typical patients are either a woman under the age of 40 or a man over the age of 60.

111
Q

Describe the pathophysiology behind myasthenia gravis

A

In most with myasthenia gravis, acetylcholine receptor antibodies are produced by the immune system. These bind to the postsynaptic neuromuscular junction receptors. This blocks the receptor and prevents the acetylcholine from being able to stimulate the receptor and trigger muscle contraction. As the receptors are used more during muscle activity, more of them become blocked up. This leads to less effective stimulation of the muscle with increased activity. There is more muscle weakness the more the muscles are used. This improves with rest as more receptors are freed up for use again.

112
Q

State 5 symptoms of myasthenia gravis

A

Extraocular muscle weakness causing double vision (diplopia), eyelid weakness causing drooping of the eyelids (ptosis), weakness in facial movements, difficulty with swallowing, fatigue in the jaw when chewing, slurred speech, progressive weakness with repetitive movements

113
Q

How do we diagnose myasthenia gravis?

A

Diagnosis can be made testing directly for the relevant antibodies:
Acetylcholine receptor (ACh-R) antibodies (85% of patients)
Muscle-specific kinase (MuSK) antibodies (10% of patients)
LRP4 (low-density lipoprotein receptor-related protein 4) antibodies (less than 5%)

A CT or MRI of the thymus gland is used to look for a thymoma.

114
Q

What is the edrophonium test?

A

Patients are given an IV dose of edrophonium chloride (or neostigmine). Normally, cholinesterase enzymes in the neuromuscular junction break down acetylcholine. Edrophonium block these enzymes and stop the breakdown of acetylcholine. As a result the level of acetylcholine at the neuromuscular junction increases. It briefly and temporarily relieves the weakness. This establishes a diagnosis of myasthenia gravis.

115
Q

How do you treat myasthenia gravis?

A

Reversible acetylcholinesterase inhibitors (usually pyridostigmine or neostigmine) increases the amount of acetylcholine in the neuromuscular junction and improve symptoms
Immunosuppression (e.g. prednisolone or azathioprine) suppresses the production of antibodies
Thymectomy can improve symptoms even in patients without a thymoma

116
Q

What is a myasthenia crisis?

A

Myasthenic crisis is a severe complication of myasthenia gravis. It can be life threatening. It causes an acute worsening of symptoms, often triggered by another illness such as a respiratory tract infection. This can lead to respiratory failure as a result of weakness in the muscle of respiration. Patients may require non-invasive ventilation with BiPAP or full intubation and ventilation.

Medical treatment of myasthenic crisis is with immunomodulatory therapies such as IV immunoglobulins and plasma exchange.

117
Q

What is bulbar palsy?

A

Bulbar relates to the medulla. Bulbar palsy is the result of diseases affecting the lower cranial nerves (VII-XII). A speech deficit occurs due to paralysis or weakness of the muscles of articulation which are supplied by these cranial nerves

118
Q

How does bulbar palsy present?

A

Lips - tremulous.
Tongue - weak and wasted and sits in the mouth with fasciculations.
Drooling - as saliva collects in the mouth and the patient is unable to swallow (dysphagia).
Absent palatal movements.
Dysphonia - a rasping tone due to vocal cord paralysis; a nasal tone if bilateral palatal paralysis.
Articulation - difficulty pronouncing r; unable to pronounce consonants as dysarthria progresses.

119
Q

How do we manage bulbar palsy?

A

Refer to neurology, admit if dysphagia is present or symptoms are rapidly progressive.

120
Q

What is radiculopathy?

A

A range of symptoms produced by the pinching of a nerve root in the spinal column, resulting in inflammation

121
Q

Give three symptoms of radiculopathy.

A

Sharp pain in the back, arms, legs or shoulders that may worsen with certain activities, even something as simple as coughing or sneezing
Weakness or loss of reflexes in the affected limbs
Numbness/paraesthesia

122
Q

What can cause radiculopathy?

A

Herniated disk, bone spurs, ossification

123
Q

How do radiculopathy and myelopathy differ?

A

Myelopathy is the compression of the spinal cord itself. When the spinal cord is involved, the symptoms can be more severe, including poor coordination, trouble walking and paralysis.

124
Q

How is radiculopathy treated?

A

Steroids, painkillers, surgery

125
Q

Give five red flag signs of spinal fracture

A

Sudden onset of severe central pain in the spine which is relieved by lying down.
Trauma
Structural deformity of the spine
Point tenderness over the vertebral body

126
Q

What is sciatica?

A

Sciatica is where the sciatic nerve, which runs from your lower back to your feet, is irritated or compressed.

127
Q

Give common causes of sciatica.

A

Slipped disc, spinal stenosis, spondylolisthesis – when one of the bones in your spine slips out of position, back injury

128
Q

Give four causes of sciatica that aren’t spine related

A

Dissecting aortic aneurysm, a posterior duodenal ulcer, nephrolithiasis, pyelonephritis

129
Q

Give red flag symptoms/signs of spinal cord compression.

A

Insidious progression
Neurological symptoms: gait disturbance, clumsy or weak hands; loss of sexual, bladder or bowel function
Neurological signs: Lhermitte’s sign, UMN signs in the lower limbs, LMN signs in the upper limbs, sensory changes

130
Q

What is Lhermitte’s sign?

A

Flexion of the neck causes an electric shock-type sensation that radiates down the spine and into the limbs

131
Q

What investigations would you order for a pt with suspected spinal cord compression?

A

Haemoglobin and haematocrit levels should be measured initially and monitored serially to monitor blood loss.
Renal function and electrolytes: dehydration.
MRI scan of the whole spine.

132
Q

Give five causes of spinal cord compression.

A

Trauma, malignancy, slipped disk, infection, RA

133
Q

What is a subarachnoid haemorrhage?

A

Bleeding into the subarachnoid space - where the cerebrospinal fluid is located - between the pia mater and the arachnoid membrane, usually due to a ruptured cerebral aneurysm.

134
Q

Describe potential symptoms of SAH.

A

Thunderclap headache, neck stiffness, photophobia, vision changes, neurological symptoms such as speech changes, weakness, seizures and loss of consciousness

135
Q

Define thunderclap headache.

A

A sudden onset occipital headache that occurs during strenuous activity such as weight lifting or sex

136
Q

Describe the epidemiology behind SAH.

A

Black patients, female patients, age 45-70

137
Q

What might you look for in the FH/SH/PMH of someone presenting with SAH?

A

Cocaine use, sickle cell anaemia, connective tissue disorders (such as Marfan syndrome or Ehlers-Danlos), neurofibromatosis, autosomal dominant polycystic kidney disease

138
Q

How do we treat SAH?

A

Nimodipine (reduce risk of vasospasm), shunt, surgery

139
Q

What causes subdural haemorrhage?

A

Subdural haemorrhage is caused by rupture of the bridging veins in the outermost meningeal layer. They occur between the dura mater and arachnoid mater.

140
Q

How would a subdural haemorrhage appear on a CT?

A

On a CT scan they have a crescent shape and are not limited by the cranial sutures (they can cross over the sutures).

141
Q

Who are subdural haemorrhages more common in?

A

The elderly, due to cerebral atrophy

142
Q

What usually causes an extradural haemorrhage?

A

Usually caused by rupture of the middle meningeal artery in the temporo-parietal region. It can be associated with a fracture of the temporal bone. It occurs between the skull and dura mater.

143
Q

How do extradural haemorrhages appear on CT?

A

On a CT scan they have a bi-convex shape and are limited by the cranial sutures (they can’t cross over the sutures).

144
Q

Describe the typical presentation of extradural haemorrhage.

A

The typical history is a young patient with a traumatic head injury that has an 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 the intracranial contents.

145
Q

How do we manage haemorrhage?

A

Immediate head CT. Check FBC and clotting. Inform neurosurgery. Correct severe HTN but avoid hypotension.

146
Q

What is anterior spinal artery syndrome?

A

A syndrome caused by ischemia of the anterior spinal artery, resulting in loss of function of the anterior two-thirds of the spinal cord

147
Q

How does anterior cord syndrome present?

A

It is characterized by a corresponding loss of motor function, loss of pain and temperature sensation, and hypotension.

148
Q

Why is anterior cord syndrome the most common spinal infarct?

A

The anterior spinal cord is at increased risk for infarction because it is supplied by the single anterior spinal artery, and doesn’t have many collateral supplies.

149
Q

What is convulsive status epilepticus?

A

A convulsive seizure which continues for a prolonged period (longer than five minutes), or when convulsive seizures occur one after the other with no recovery between.

150
Q

Give RFs for status epilepticus.

A

Age under 5 years or elderly age, genetic predisposition, intellectual disability and structural brain pathology

151
Q

What is the main differential for status epilepticus?

A

Pseudo-status epilepticus which is non-epileptic attacks with a psychological basis. See if tonic-clonic or not.

152
Q

How is status epilepticus treated in the community?

A

DR CABCDE, buccal midazolam as first-line treatment for prolonged or repeated seizures in the community or rectal diazepam if preferred or if buccal midazolam is not available; IV lorazepam if possible.

153
Q

What is the second line treatment of status epilepticus in the hospital?

A

Administer IV phenobarbital or phenytoin as second-line treatment. Fosphenytoin (a prodrug of phenytoin) can be given more rapidly and, when given intravenously, causes fewer injection-site reactions than phenytoin

154
Q

What is Guillain-Barré syndrome?

A

An “acute paralytic polyneuropathy” that affects the peripheral nervous system. It causes acute, symmetrical, ascending weakness and can also cause sensory symptoms

155
Q

What causes Guillain-Barré syndrome?

A

It is usually triggered by an infection and is particularly associated with to campylobacter jejuni, cytomegalovirus and Epstein-Barr virus.

156
Q

Describe the pathophysiology behind Guillain-Barré syndrome.

A

Guillain-Barré is thought to occur due to a process called molecular mimicry. The B cells of the immune system create antibodies against the antigens on the pathogen that causes the preceding infection. These antibodies also match proteins on the nerve cells. They may target proteins on the myelin sheath of the motor nerve cell or the nerve axon.

157
Q

How is Guillain-Barré syndrome diagnosed?

A

Clinically, using the Brighton criteria.

158
Q

How would a LP look in a pt with Guillain-Barré syndrome?

A

Raised protein with a normal cell count and glucose

159
Q

How is Guillain-Barré syndrome managed?

A

IV immunoglobulins
Plasma exchange (alternative to IV IG)
Supportive care
VTE prophylaxis (pulmonary embolism is a leading cause of death)

160
Q

What is coma?

A

A state of profound unconsciousness caused by disease, injury, or poison. The patient is unresponsive and cannot be roused.

161
Q

What is stupor?

A

Similar to coma in that responsiveness is greatly diminished. However, the person can still be partially roused by some stimuli, such as pain

162
Q

What is obtundation?

A

Reduced awareness to surroundings. The patient needs constant stimulation to remain awake.

163
Q

What is drowsiness?

A

This is similar to obtundation and probably represents a lesser loss of consciousness

164
Q

What does a GCS of less than/equal to eight show?

A

A severe reduction in consciousness and the patient is unlikely to be able to maintain their airway spontaneously, thus should be intubated and ventilated

165
Q

What are myopathies?

A

General term referring to any disease that affects the muscles that control voluntary movement in the body

166
Q

What is the main feature of myopathy?

A

The hallmark symptom of myopathy (and neuromuscular disease) is weakness, typically affecting proximal muscle groups

167
Q

What is epilepsy?

A

The tendency to have seizures

168
Q

Define seizure?

A

Excessive, unsynchronised neuronal discharges in the brain cause paroxysmal changes in behaviour, sensation or cognitive processes.

169
Q

How do we use EEG in epilepsy diagnosis?

A

It can show typical patterns in different forms of epilepsy and support the diagnosis

170
Q

How do we use MRI in epilepsy diagnosis?

A

An MRI brain can be used to visualise the structure of the brain. It is used to diagnose structural problems that may be associated with seizures and other pathology such as tumours

171
Q

Describe a tonic-clonic seizure.

A

There is loss of consciousness and tonic (muscle tensing) and clonic (muscle jerking) episodes. Typically the tonic phase comes before the clonic phase. There may be associated tongue biting, incontinence, groaning and irregular breathing.

172
Q

How does a person typically feel after a generalised tonic-clonic seizure?

A

After the seizure there is a prolonged post-ictal period where the person is confused, drowsy and feels irritable or depressed.

173
Q

How do we manage generalised tonic-clonic seizures?

A

First line: sodium valproate

Second line: lamotrigine or carbamazepine

174
Q

Where do focal seizures begin?

A

The temporal lobes

175
Q

How do focal seizures present?

A

Hallucinations
Memory flashbacks
Déjà vu
Doing strange things on autopilot

176
Q

How do we manage focal seizures?

A

First line: carbamazepine or lamotrigine

Second line: sodium valproate or levetiracetam

177
Q

How do we manage absence seizures?

A

First line: sodium valproate or ethosuximide

178
Q

What are atonic seizures?

A

Atonic seizures are also known as “drop attacks”. They are characterised by brief lapses in muscle tone. These don’t usually last more than 3 minutes.

179
Q

What might atonic seizures indicate?

A

Lennox-Gastaut syndrome

180
Q

How do we manage atonic seizures?

A

First line: sodium valproate

Second line: lamotrigine

181
Q

What are myoclonic seizures?

A

Myoclonic seizures present as sudden brief muscle contractions, like a sudden “jump”. The patient usually remains awake during the episode.

182
Q

How do we treat myoclonic seizures?

A

First line: sodium valproate

Other options: lamotrigine, levetiracetam or topiramate

183
Q

How does sodium valporate work?

A

It works by increasing the activity of GABA, which has a relaxing effect on the brain.

184
Q

Give four side effects of sodium valporate.

A

Teratogenic so patients need careful advice about contraception
Liver damage and hepatitis
Hair loss
Tremor

185
Q

Give four side effects of carbamazepine

A

Agranulocytosis
Aplastic anaemia
Induces the P450 system so there are many drug interactions

186
Q

How does GBS present?

A

a

187
Q

How do we treat brain abscess?

A

Drainage, abx

188
Q

How does brain abscess present?

A

a

189
Q

Describe the symptoms of polio

A

a

190
Q

What causes polio?

A

a

191
Q

How do we treat polio?

A

a

192
Q

A pt presents with a UMN lesion. Their gait is affected. What would you expect to see?

A

Hemiplegic/diplegic gait

P3A Med (9 decks)

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