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Phase 3a > Neurology > Flashcards

Neurology Flashcards

1
Q

Name all the lobes of the cerebrum

A

Frontal
Parietal
Temporal
Occipital

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2
Q

What is a cortical association area?

A

Areas in each lobe where information from different modalities are collated for processing

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3
Q

What does the frontal lobe do?

A

The association areas of the frontal lobe are responsible for higher intellect, personality, mood, social conduct and language. Contains Broca’s area.

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4
Q

What does the parietal lobe do?

A

Areas contribute to control of language and calculation on the dominant side and visuospatial functions on the non dominant side

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5
Q

What does the temporal lobe do?

A

Areas are associated with memory and language, including hearing as it is the location of the primary auditory cortex. Contains Wernicke’s area.

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6
Q

What does the occipital lobe do?

A

cortical association area is responsible for vision. Contains the primary and secondary visual cortex.

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7
Q

What is MND?

A

An umbrella term for several different diagnoses. Degenerative disease characterised by axonal degeneration of neurones in the motor cortex, cranial nerve nuclei and anterior horn cells

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8
Q

What are the cranial nerve nuclei?

A

Collections of neurons in the brain stem that are associated with one or more of the cranial nerves

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9
Q

What does the corticospinal cord do?

A

Corticospinal tract involved in fine and voluntary motor function eg waling and talking but also reading, writing and typing. Most corticospinal tract fibres decussate to the contralateral side from where they originated. So if they originated from the right side of the brain, will cause movement in the left side of the body.

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10
Q

What are the different types of MND?

A

Amytrophic lateral sclerosis
Progressive muscular atrophy
Primary lateral sclerosis
Progressive bulbar palsy

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11
Q

Describe some features of ALS

A

Asymmetric onset of weakness in upper or lower limb
Mix of UMN + LMN signs
UMN signs: predominantly affects corticospinal tracts. Muscle weakness, spasticity, hyperreflexia and clonus
LMN signs: affecting anterior horn cells. Weakness, muscle atrophy and fasciculation
Increased plantar responses
Neck flexion weakness
Corticobulbar signs eg brisk jaw jerk

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12
Q

Describe some features of progressive bulbar palsy

A

More common in older women
Onset with dysarthria and/or dysphagia
Limb involvement later on

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13
Q

Describe some features of progressive muscular atrophy

A

LMN weakness of arms or legs
Most develop bulbar symptoms

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14
Q

Define epilepsy

A

An umbrella term for a condition where there is tendency to have seizures. Seizures are episodes of abnormal electrical activity in the brain.

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15
Q

What are the causes of epilepsy?

A

Genetic
Structural eg congenital malformation, cerebrovascular disease, tumour
Metabolic
Immune
Infectious eg HIV
Unknown
Alcohol
Post-traumatic

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16
Q

How are seizures categorised?

A

Into focal vs generalised

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17
Q

What is a focal seizure?

A

It is when the affected area is limited to one hemisphere or lobe. Often start in temporal lobe and can affect hearing, speech, memory or emotions. Can present with hallucinations, memory flashback, deja vu. Can also be with or without impaired awareness.

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18
Q

What is a generalised seizure and what types are there?

A

Seizure where both hemispheres of the brain are affected. Subcategories include:
-tonic
-atonic
-clonic
-myoclonic
-absence

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19
Q

What is a tonic seizure?

A

Muscles become stiff and flexed, causing the patient to fall backwards

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20
Q

What is an atonic seizure?

A

Also called drop attacks where the patient’s muscles suddenly become relaxed and floppy and patient usually falls forwards. Typically begin in childhood. May indicate Lennox-Gastaut syndrome

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21
Q

What is a clonic seizure?

A

violent muscle contractions/convulsions

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22
Q

What is a tonic-clonic seizure?

A

Loss of consciousness and tonic (muscle tensing) and clonic (muscle jerking) episodes. Might be tongue biting or incontinence

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23
Q

What is a myoclonic seizure?

A

Short muscle twitches with patient normally awake. Typically occur in kids as juvenile myoclonic epilepsy

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24
Q

What is an absence seizure?

A

Impaired awareness or responsiveness. Patient becomes blank and stares in space. Motor abnormalities may be minor or not present.

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25
Q

What is West syndrome?

A

a rare disorder staring in infancy at around 6 months where the child suffers from clusters of full body spasms. Prognosis is poor where 1/3 die by age 25. Typical EEG findings show hypsarrhythmia. Also known as infantile spasms.

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26
Q

What are some triggers for seizures in epilepsy?

A

Alcohol
Fatigue
Sleep deprivation
Infections
Hypoglycaemia
Stress
Strobe lighting
(rarely) hot water or reading

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27
Q

Describe the clinical features of juvenile myoclonic epilepsy (JME)

A

Onset before 30
Myoclonic jerks in the morning eg dropping things in the morning
Typical absences
Generalised tonic clonic seizures

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28
Q

What is the prodromal phase?

A

Confusion, irritability or mood disturbance just before the onset of seizures

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29
Q

What is the early ictal phase?

A

The aura or warning felt before the seizure. Can include sensory, cognitive, emotional or behaviour changes

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30
Q

What is the ictal phase?

A

The seizure itself

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31
Q

What is the post ictal phase?

A

Confused, drowsy or irritable after a seizure.

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32
Q

What are the investigations (and results ) for epilepsy?

A

EEG: can show different patterns in different forms of epilepsy
MRI brain: can diagnose or rule out structural problems eg tumours or cerebrovascular disease
ABG: rule out metabolic acidosis with raised lactate
ECG: exclude heart problems –> cardiac arrhythmia eg long QT syndrome
Blood electrolytes: eg sodium, potassium and calcium all causing seizures
Blood glucose: for hypoglycaemia
Blood/urine cultures: rule out sepsis and infection

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33
Q

What are the investigations (and results ) for epilepsy?

A

EEG: can show different patterns in different forms of epilepsy
MRI brain: can diagnose or rule out structural problems eg tumours or cerebrovascular disease
ABG: rule out metabolic acidosis with raised lactate
ECG: exclude heart problems –> cardiac arrhythmia eg long QT syndrome
Blood electrolytes: eg sodium, potassium and calcium all causing seizures
Blood glucose: for hypoglycaemia
Blood/urine cultures: rule out sepsis and infection

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34
Q

What should a patient avoid doing if they have seizures?

A

Driving: DVLA must be informed and can only drive if been seizure free for a year
Avoid swimming alone, walking or running alone or going somewhere remote alone
Take showers rather than baths to avoid drowning

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35
Q

What is the treatment for generalised tonic clonic seizures?

A

1st line: sodium valproate OR carbamazepine if female

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36
Q

What is the treatment for focal seizures?

A

1st line: lamotrigine or carbamazepine

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37
Q

What is the treatment for myoclonic seizures?

A

1st line: sodium valproate OR lamotrigine

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38
Q

What is the treatment for absence seizures?

A

1st line: sodium valproate
2nd line: lamotrigine

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39
Q

Rare side effect of lamotrigine?

A

Stevens-Johnson syndrome:
Develops up to 2 months after beginning lamotrigine. Prodromal viral like illness precedes rapid onset red rash which rarely affects the soles, palms or scalp

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40
Q

Describe some features of progressive muscular atrophy

A

LMN weakness of arms or legs
Most develop bulbar symptoms

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41
Q

When should anti-epileptic drug treatment be started after a patient’s first seizure?

A

Patients should be referred to a specialist clinic and anti-epileptic drugs should only be started after this review, EXCEPT
1. when seizure activity is noted on an EEG
2. in the presence of neurological deficit
3. presence of a structural brain abnormality
4. patient, parent or carer finds the occurrence of another seizure unacceptable

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42
Q

Common signs and symptoms in MND

A

Mixed UMN and LMN signs
Brisk reflexes
Upgoing plantar responses
Fasciculations
Dysarthria/dysphagia
Muscle wasting esp in small hand muscles
Reduced tone
Progressive weakness
Clumsiness
Fatigue
Falls
Speech and wallow issues

Sensory and extraocular symptoms not present

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43
Q

What are the investigations for MND (and their results)?

A

MND is a clinical diagnosis –> definite MND is UMN + LMN signs in 3 regions

Investigations can rule out other causes of symptoms:
- Electromyography (EMG): will show evidence of fibrillation potentials
- nerve conduction studies
- MRI should be normal in MND
- Lumbar puncture to rule out inflammatory or infectious causes

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44
Q

What is the management for someone with MND?

A

Riluzole: prolongs survival ~3 months and might protect motor neurons from glutamate induced damage. Helps patients and families psychologically.
Nutrition: consider PEG if patient unable to take medication or eat
Involvement of MDT: specialist nurse, physio, orthotics, SALT, dieticians, resp team, later stages palliative care
Depression/emotional symptoms: psychological support and medication eg citalopram
Resp support: BiPAP can help patients with reduced FVC

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45
Q

Define Huntington’s disease

A

It is an autosomal dominant neurodegenerative disease caused by multiple repeats (>36) of the CAG trinucleotide.

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46
Q

What is the pathophysiology of Huntington’s Disease?

A

A genetic mutation on the HTT gene on chromosome 4. CAG codes for glutamine so patients have more glutamines in a row in the huntingtin protein. The mutated proteins accumulate in the neuronal cells of the caudate and putamen of the basal ganglia and lead to neuronal cell death. If enough neurones die, there is a loss in brain tissue volume and expansion of the lateral ventricles.

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47
Q

What does genetic ‘anticipation’ mean?

A

Anticipation is a feature of trinucleotide disorders eg in Huntington’s. The expanded CAG repeat affects DNA replication. DNA polymerase loses track of which CAG it’s on so can add extra CAGs leading to repeat expansion. This means successive generations tend to have more repeats in the gene leading to earlier age of onset and increased severity of disease

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48
Q

What are the signs and symptoms of Huntington’s Disease?

A

patient’s are asymptomatic until symptoms begin aged 30-50
Begins with prodromal phase- cognitive, psychiatric or mood problems
Chorea (abnormal, involuntary movements)
Eye movements
Dysarthria
Dysphagia
Dementia

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49
Q

What are the investigations for Huntington’s Disease?

A

Diagnosis is made using genetic testing for the faulty gene and to identify the number of CAG repeats

MR or CT scans can show caudate or striatal atrophy in later disease as not normally present in very early disease.

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50
Q

What is the management for Huntington’s Disease?

A

Post test counselling: to help patients cope with diagnosis
Genetic counselling: to discuss relatives, pregnancy and children
MDT: physio, OT, speech & language
Advanced directives and end of life care planning
Antipsychotics eg olanzapine and benzodiazepines eg diazepam can help treat disordered movement

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51
Q

Define Guillain-Barre syndrome?

A

It is an acute inflammatory neuropathy. It is classified according to symptoms and divided into axonal and demyelinating forms. It is a neurological emergency

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52
Q

What are the causes of GBS?

A

Two thirds are preceded by a GI or URT infection with the most commonly associated organisms –> campylobacter jejuni, EBV, cytomegalovirus, haemophilus influenzae

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53
Q

What are the four subtypes of GBS?

A

Acute inflammatory demyelinating neuropathy: most common and affects the myelin sheath of affected nerves
Acute motor axonal neuropathy: damages the axons of motor neurons specifically. Presents with purely motor symptoms
Acute motor sensory axonal neuropathy: affects axons of both motor and sensory neurones.
Miller- Fisher syndrome: antibodies against the GQlb ganlioside and associated with a triad of opthalmoplegia, ataxia and arreflexia.

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54
Q

What are the signs and symptoms of GBS:

A

progression is subacute, with symptoms developing over a few weeks with the peak around 2-3 weeks of onset
Signs:
Reduced sensation in affected limbs, symmetrical weakness in lower limbs first with weakness normally ascending, ataxia with hyporeflexia, autonomic dysfunction eg tachycardia, hypertension, postural hypotension, respiratory distress in severe cases, cranial nerve involvement is normally facial or bulbar eg facial droop

Symptoms:
Tingling and numbness in hands and feet preceding weakness, symmetrical and progressive usually ascending weakness, unsteady when walking, back and leg pain, SOB, facial weakness and speech problems.

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55
Q

What are the investigations to diagnose GBS?

A

Bloods:
-U&Es: rule out other electrolyte abnormalities resulting in neuropathic symptoms
-B12: deficiency can cause neurological features
-TFTs: rule out hypothyroidism as cause of weakness
-LFTs: elevation of hepatic enzymes is associated with more severe disease
-anti-ganglioside antibodies: to differentiate between GBS types eg Miller Fisher
LP: elevated CSF protein with normal cell count
Nerve conduction studies: not required for diagnosis, findings will suggest demyelination
MRI brain/spinal cord: rule out other causes

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56
Q

How is GBS managed?

A

Disease modifying treatment:
First line is now IV immunoglobulin for 5 days –> can also do plasma exchange of 5 treatments of 2-3L over 2 weeks within the first 4 weeks of symptom onset

Supportive management:
DVT prophylaxis
Physiotherapy
ICU support for those that develop severe resp issues
Pain relief eg amitriptyline or gabapentin

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57
Q

Define myasthenia gravis?

A

A chronic autoimmune disorder of the post synaptic membrane at the neuromuscular junction in the skeletal muscle. Antibodies against the nicotinic acetylcholine receptor are present.

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58
Q

What is the pathology of Myasthenia Gravis?

A

Circulating autoantibodies against the acetylcholine receptor lead to fewer available binding sites for the acetylcholine receptor at the post synaptic membrane on the muscle, leading to weakness.

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59
Q

What are the signs and symptoms of myasthenia gravis?

A

Painless muscle weakness that gets worse on exercise and improves on rest.
Ptosis that is exacerbated when looking up
Myasthenic snarl- snarling expression when trying to smile
Proximal muscle weakness with fatigability
Lethargy
Diplopia
Slurred speech
Dysphagia
Fatigue in jaw when chewing
Shortness of breath –> myasthenic crisis!

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60
Q

What are the investigations for myasthenia gravis?

A

Serum AChR antibody test –> highly specific
Nerve stimulation –> sensitive in 50-60% of cases showing a decremental muscle response
CT thorax: all patients should have a Ct chest to rule out a thymoma (common for those with thymoma to develop MG)
Thyroid function: higher prevalence of autoimmune thyroiditis
Tensilon (endrophonium) test: use a rapid onset cholinesterase inhibitor. If there is improvement in a muscle that can be tested objectively, the test is positive –> can be difficult to assess in borderline cases plus can have cardiac side effects so full resuscitation should be available

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61
Q

What is the management of Myasthenia Gravis?

A

1st: Pyridostigmine: cholinesterase inhibitor. side effects- abdo pain and diarrhoea due to effects on muscarinic smooth muscle NMJ. Max dose is 300mg a day. 2-4-6 regime used
2nd: Prednisolone: used in patients who aren’t controlled well on pyridostigmine and are unsuitable for thymectomy.
3rd: azathioprine if symptoms not controlled on prednisolone

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62
Q

What is the management of a myasthenic crisis?

A

IV immunoglobulins
Intubation
Corticosteroids to be used as an adjunct

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63
Q

What is mononeuropathy?

A

Refers to the damage or dysfunction of a single peripheral nerve including any cranial nerve, spinal nerve or nerve branch that connects the CNS to the rest of the body. To of the most common are cubital tunnel and carpital tunnel syndrome

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64
Q

What are the common symptoms of a mononeuropathy?

A

Cary depending on the affected nerve and underlying cause but normally:
Sensory –> numbness, pain, tingling
Motor –> weakness, atrophy, loss of coordination

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65
Q

What are the different types of mononeuropathy?

A

Fixed mononeuropathy
Transient mononeuropathies
Non compression related

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66
Q

What are the causes of the different types of mononeuropathy?

A

Fixed mononeuropathy: nerve compression against a hard surface, entrapment of nerves in narrow anatomical spaces
Transient mononeuropathies: repetitive actions that cause trauma to neurons
Non compression related: infections, radiation, cold

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67
Q

What is anterior spinal cord syndrome?

A

Also known as anterior spinal artery syndrome. It is when the anterior spinal artery becomes occluded (for whatever reason) leading to the infarction of the anterior two third of the cord. Any damage that takes place is bilateral bc there is only spinal artery.

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68
Q

What are the signs and symptoms of anterior spinal cord syndrome?

A

There will be a loss of motor function below the level of the lesion with bilateral damage to the corticospinal tracts
There will be loss of pain and temperature sensation with vibration and proprioception preserved

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69
Q

How is anterior spinal cord syndrome diagnosed?

A

MRI imaging would show features of acute spinal cord ischaemia
LP: to rule out infection, MS etc
Echocardiogram: rule out sources of embolism eg infective endocarditis

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70
Q

What are the ascending tracts?

A

The neural pathways by which sensory information from the peripheral nerves is transmitted to the cerebral cortex. They are divided into the type of information they transmit –> conscious or unconscious

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71
Q

What are the conscious and unconscious tracts made up of?

A

Conscious tracts: comprised of the dorsal column medial lemniscal pathway and the anterolateral system
Unconscious tracts: comprised of the spinocerebellar tracts

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72
Q

What does the dorsal column medial lemniscal pathway do?

A

carries the sensory modalities of fine touch, vibration and proprioception. The information travels via the dorsal (posterior) columns in the spinal cord.

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73
Q

Define extradural (epidural) haemorrhage?

A

Arterial blood collects between the skull and the periosteal layer of the dura. The causative vessel is normally the middle meningeal artery tearing as a consequence of trauma.

Head injury with instant LOC, followed by a lucid period and then progressive decline in GCS

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74
Q

What are the risk factors for extradural haemorrhage?

A

Head injury
Hypertension
Aneurysms
Ischaemic stroke can progress to haemorrhage
Brain tumours
Anticoagulants eg warfarin

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75
Q

What are the signs and symptoms of extradural haemorrhage?

A

Reduced GCS
Headaches
Vomiting
Confusion
Seizures
Pupil dilatation if bleeding continues

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76
Q

What are the investigations for extradural haemorrhage?

A

CT Head: hyperdense mass that looks more white than the surrounding healthy brain tissue. They cause blood to build up between the outer layer of the dura mater and the skull, pushing on the brain to form a biconvex shape.
FBC & clotting
Skull X-Ray: may show skull fracture

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77
Q

What is the management for extradural haemorrhage?

A

Consider intubation, ventilation and ICU if reduced consciousness
Correct any clotting abnormality
Mannitol: reduces raised ICP

Surgery:
- burr hole over pterion to ensure further haemorrhage escapes and doesn’t expand the clot further
-craniotomy –> part of skull is removed to remove accumulate blood below
-ligation of bleeding vessel

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78
Q

What is a subdural haemorrhage?

A

Bleeding below the dura mater- damage occurs between dura and the arachnoid mater. Bleeding tends to be mixed arterial and venous. Results from damage to the cerebral veins as they empty into the dural venous sinuses

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79
Q

What are the causes of a subdural haemorrhage?

A

Rupture of bridging veins due to brain atrophy due to age or alcohol use causing the vein walls to thin out.

Trauma/ injury –> falls, shaken baby syndrome or acceleration-deceleration injury seen in RTAs

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80
Q

What are the general risk factors for subdural haemorrhage?

A

Head injury
Brian atrophy
Alcohol abuse
Hypertension
Aneurysms
Ischaemic stroke
Brain tumours
Anticoagulants eg warfarin

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81
Q

What are the three types of subdural haemorrhage?

A

Acute subdural: causes symptoms within 2 days, occurs after high impact injury, haemorrhage is arterial and venous
Subacute subdural: causes symptoms between 3-14 days
Chronic subdural: causes symptoms after 15 days

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82
Q

What are the signs and symptoms of a subdural haemorrhage?

A

Reduced GCS immediately after the injury or in the days and weeks afterwards
Headaches
Vomiting
Seizures
Focal neurological symptoms –> muscle weakness, unequal pupils, hemiparesis or sensory problems

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83
Q

What are the investigations for a subdural haemorrhage?

A

CT Head: bleeding is between dura and arachnoid so subdural haematomas follow the contour of the brain and form a crescent shape, and can cross suture lines
-acute subdural: hyperdense white mass
-chronic subdural: hypodense less white mass

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84
Q

What is the management of subdural haemorrhage?

A

Consider intubation, ventilation and ICU care if reduced consciousness
Correct and clotting abnormality
Mannitol: to reduced any raised ICP

Acute:
-emergency trauma craniotomy with a large flap to expose haematoma for evacuation and haemostasis
-cerebral swelling is common and may require frontal or temporal lobectomy and bone flap removal

Chronic:
-consider dexamethasone if treatment non surgical
-cortical compression, midline shift and contralateral hydrocephalus indicate need for surgery
-burr hole drainage +/- subdural drain

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85
Q

What is a subarachnoid haemorrhage?

A

A type of intercranial haemorrhage characterised by blood in the subarachnoid space?

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86
Q

What are the causes of subarachnoid haemorrhage?

A

Trauma
Atraumatic/spontaneous SAH:
-berry aneurysm arising at points of arterial bifurcation in the circle of Willis –> junction between ACA and anterior cerebral v common
Arteriovenous malformation
Mycotic aneurysm
Perimesencephalic –> venous bleeding with normal CT
Vertebral artery dissection

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87
Q

What are the risk factors for subdural arachnoid haemorrhage?

A

Age
Hypertension
Smoking
Alcohol excess
Cocaine use
Family history
Polycystic kidney disease
Connective tissue disorders
Neurofibromatosis

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88
Q

What is the pathophysiology of subarachnoid haemorrhage?

A

Leads to a pool of blood under the arachnoid mater leading to increased intercranial pressure. Pressure on nearby tissue cells leads to cell death
Blood vessels in pools of blood go into vasospasm.
Hydrocephalus occurs –> blood irritates the meninges and causes inflammation, leading to scarring of the surrounding tissues. The scar tissue obstructs the normal outflow of cerebrospinal fluid, causing fluid to build up which dilates the ventricles at the centre of the brain.

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89
Q

What are the signs and symptoms of subarachnoid haemorrhage?

A

Signs:
-3rd nerve palsy: aneurysm in PCA will press on 3rd nerve (oculomotor) causing a palsy with fix dilated pupil.
-6th nerve palsy is a non-specific sign indicated raised ICP

Symptoms:
-headache (severe with sudden onset/thunderclap/occipital)
-meningism eg photophobia and neck stiffness
-vision changes
-nausea and vomiting
-speech changes
-seizures
-weakness
-confusion
-coma

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90
Q

What are the investigations for subarachnoid haemorrhage?

A

FBC
Serum glucose
Clotting screen
CT Head non contrast –> diagnostic and can show blood in the basal cisterns
ECG –> assess for arrhythmias, ischaemia and ST elevation
LP –> (if CT negative but clinical suspicion still indicating SAH) RBCs/xanthochromia with normal or raised opening pressures
CT angiogram

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91
Q

What is the management of subarachnoid haemorrhage?

A

Nimodipine: CCB that is used to prevent vasospasm
Intervention: 1st line is endovascular coiling and 2nd line is surgical clipping via craniotomy
Strict bed rest with bed at 45 degrees
Analgesia

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92
Q

What is giant cell arteritis?

A

It is a granulomatous vasculitis of large and medium sized arteries. It mostly affects branches of the external carotid. More commonly affects women and those >55 plus associated with polymyalgia rheumatica

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93
Q

What is the pathophysiology of giant cell arteritis?

A

Granulomatous inflammation occurs along the vessel walls. Leads to intimal thickening and a narrowed vascular lumen.
Common arterial distributions –>
-superficial temporal artery
-mandibular artery
-opthalmic artery

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94
Q

What are the signs and symptoms of GCA?

A

Signs:
-superficial temporal artery tenderness
-absent temporal artery pulse
-reduced visual acuity
-pallor of the optic disc

Symptoms:
-severe unilateral persistent headache
-blurred vision/amaurosis fugax
-scalp pain (hair brushing pain)
-jaw claudication
-systemic symptoms eg fever, muscle aches, weight loss. loss of appetite

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95
Q

What are the investigations (and their results) for GCA?

A

CRP: elevated
ESR: elevated
Temporal artery biopsy: histopathologically shows granulomatous inflammation, multi-nucleated giant cells (in 50%), inflammatory infiltrate may be focal and segmental
Vascular ultrasonography: may show wall thickening (halo sign), stenosis or occlusion. Non-compressible halo sign is the finding that most indicates GCA

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96
Q

What is the diagnostic criteria for a positive diagnosis of GCA?

A

3 or more criteria should be met:
-50 years +
-new onset headache
-temporal artery abnormality
-elevated ESR 50mm/h or more
-abnormal temporal artery biopsy

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97
Q

What is the management for GCA?

A

1st line: corticosteroid. 40-60mg prednisolone daily if no visual symptoms. IV methylprednisolone is required for visual symptoms
Aspirin –> protects against ischaemic cranial complications

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98
Q

Define encephalitis

A

Inflammation of the brain parenchyma associated with neurological dysfunction eg altered consciousness, seizures, personality changes, cranial nerve palsies, speech problems and motor/sensory deficits. Result of direct inflammation of the brain tissue (NOT inflammation of the meninges). Causes can be infectious or non-infectious.

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99
Q

What are the causes of encephalitis?

A

Viral:
-Herpes (most common cause!)
-EBV
-CMV
-Polio
-Coxsackie
-HIV

Bacterial:
-Neisseria meningitidis
-TB
-syphilis

Fungal:
-Cryptococcus

Parasitic:
-Toxoplasmosis
-Cysticercosis

Paraneoplastic:
-Anti NMDA (ovarian teratoma)
-Anti voltage gated potassium channel

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100
Q

What are the signs and symptoms of encephalitis?

A

Signs:
Pyrexia (viral?), reduced GCS, focal neurological deficit –> aphasia, hemiparesis, cerebellar signs

Symptoms:
Fever, headache, fatigue, confusion, seizures, memory disturbance, psychotic behaviour, personality change

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101
Q

What is the clinical presentation of someone with Anti-NMDA encephalitis?

A

Likely female (80%)
Likely <50 years old
Prodromal viral like syndrome common
Rapid change in behaviour –> psychiatric symptoms of anxiety, agitation, delusion, paranoia, catatonia, visual/auditory hallucinations
Seizures
Memory loss
Autonomic instability
Central hypoventilation
Decreased consciousness

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102
Q

What are the investigations for encephalitis?

A

Blood tests:
-FBC, CRP, U&Es
-throat swab for viral organisms
-HIV serology

CT/MRI head –> MRI preferred and will show evidence of inflammation in the medial, temporal and inferior frontal lobes in HSV encephalitis

Lumbar puncture + CSf investigations:
-PCR for common viral infections including HSV
-Culture: identify or rule out bacterial causes
-identify specific antibodies eg NMDA receptor antibody

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103
Q

What is the management for encephalitis?

A

Viral encephalitis:
-aciclovir for 14 days
-steroids if evidence of raised ICP
-if cuased by syphilis use benzylpenicillin

Autoimmune/paraneoplastic:
-remove tumour if present eg anti-NMDA can be caused by ovarian teratoma
-first line is IV steroids and immunoglobulins
-immune modulating therapy –> rituximab or cyclophosphamide

Supportive care

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104
Q

Define multiple sclerosis

A

An inflammatory demyelinating disease characterised by the presence of episodic neurological dysfunction in at least two areas of the CNS, and separated in time and space.

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105
Q

What is the pathophysiology of MS?

A

The immune system attacks the myelin sheath surrounding the axons. It is a type IV hypersensitivity reaction because T cells release cytokines. Damage occurs to the oligodendrocytes which leaves behind areas of plaque/sclera.

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106
Q

What are the subtypes of MS?

A

Relapsing-remitting: episodic flare ups separated by periods of remission, although there isn’t full recovery after flare ups so disability increases over time

Secondary progressive: the disease starts off as relapsing remitting until symptoms begin to get progressively worse with no periods of remission

Primary progressive: symptoms get progressively worse with no periods of remission

Progressive relapsing: one constant attack with more severe attacks during which the disability progresses faster

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107
Q

What are the signs and symptoms of MS?

A

Signs:
-optic neuritis= loss of vision in one eye, pain on eye movement, pale optic disk and inability to see red, relative afferent pupillary defect
-double vision due to lesions on sixth cranial nerve
-UMN inc spasticity, hypertonia, hyperreflexia
-cerebellar signs eg ataxia and tremor
-sensory loss due to demyelination of spinothalamic or dorsal columns
-trigeminal neuralgia

Symptoms:
-blurred vision and red desaturation
-numbness/tingling
-weakness
-bowel and bladder dysfunction
-Lhermitte’s phenomenon= electric shock sensation on neck flexion
-uhtoff’s phenomenon= worsening of symptoms during higher temperatures

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108
Q

What are the investigations for MS?

A

MRI brain and spine: demyelinating plaques (Dawson’s fingers are flame like around the ventricles). High signal T2 lesions. New lesions will enhance with contrast and older lesions will not.

Lumbar puncture: oligoclonal bands found in the CSF not serum.

Visual evoked potentials: responses recorded to a visual stimulus using electrodes –> delayed velocity but a normal amplitude

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109
Q

What is the diagnostic criteria for MS?

A

McDonald Criteria

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110
Q

What is included in the McDonald Criteria?

A

2 or more relapses AND EITHER:

-objective clinical evidence of 2 or more lesions OR
-objective clinical evidence of one lesion with reasonable history of previous relapse

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111
Q

How do you manage an MS relapse?

A

Steroids: oral or IV methylprednisolone
Plasma exchange: removes the antibodies

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112
Q

What is the maintenance management of MS?

A

Beta interferon: decreases the level of inflammatory cytokines
Monoclonal antibodies: eg alemtuzumab
Glatiramer acetate: immunomodulator
Fingolimod: sphingosine-1-phosphate receptor modulator

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113
Q

How do you manage the complications of MS?

A

Spasticity: physiotherapy, baclofen/gabapentin
Neuropathic pain: gabapentin or amitriptyline
Bladder dysfunction: catheter or anti-cholinergic oxybutynin
Depression: SSRIs

114
Q

What is meningitis?

A

Inflammation of the leptomeninges (the arachnoid and pia mater). Usually due to bacterial, viral or fungal infection.

115
Q

What are the bacterial causes of meningitis?

A

Bacterial –> most common are N Meningitidis and S Pneumoniae
-Neonatal: Group B strep, e coli
-Children: N Meningitidis, S Pneumoniae, H Influenzae
-Adults: N Meningitidis, S Pneumoniae
-Immunocompromised: Listeria Monocytogenes

116
Q

What are the viral causes of meningitis?

A

Enteroviruses: coxsackie and echovirus
Herpes simplex
Varicella zoster

117
Q

What are the fungal and other causes of meningitis?

A

Cryptococcus neoformans
Candida

Can also be caused by cancer, autoimmune disease, trauma or drugs

118
Q

What is the likely causative organism if the patient has seizures?

A

Strep. Pneumoniae
Haemophilus influenzae

119
Q

What is the likely causative organism for meningitis during pregnancy/childbirth?

A

Listeria monocytogenes

120
Q

What are the signs and symptoms of meningitis?

A

Presenting features of headache, photophobia, neck stiffness and fever

-cranial palsies of III, IV, VI, VII
-focal neurological deficits
-seizures usually in S Pneumoniae and H Influenzae
-Purpura (non blanching) N Meningitidis
-septic shock N Meningitidis

121
Q

What are the investigations for meningitis?

A

Blood culture –> positive in bacterial cases
Blood glucose
Whole blood PCR for N meningitidis
CXR for signs of TB (cause of meningitis)
Lumbar puncture –> CSF gram stain, CSF culture, CSF PCR

122
Q

What is the management of meningitis before the identification of the causative organism?

A

Meningitis with typical rash: IV 2.4 benzylpenicillin 4 hourly. IV chloramphenicol if penicillins contraindicated

Meningitis without typical rash: IV cefotaxime 2g 6 hourly or IV ceftriaxone 2g 12 hourly and ADD IV ampicillin if >50 to cover listeria

123
Q

What are the LP findings for the different causes of meningitis?

A

Bacterial: CSF increased (over 200mmH2O), 100-60,000 WBC/L (mainly neutrophils), 0.5-5 g/L of protein (this is raised!), <40% blood glucose (this is low)

TB: CSF raised, 10-500 lymphocytes, 0.5-5g/L protein (raised!), les than <40% blood glucose

Fungal meningitis: raised CSF, 25-500 WBC mainly lymphocytes, 0.5-5g/L protein, reduced glucose

Viral: normal or raised CSF, raised lymphocytes, 0.5-2g/l of proteins (less than in the other causes), NORMAL blood glucose

124
Q

Compare what the CSF looks like from a lumbar puncture for bacterial vs viral meningitis?

A

Bacterial: cloudy, high protein, low glucose, high neutrophil count
Viral: clear, mildly raised or normal protein, normal glucose, high lymphocyte count

125
Q

What antibiotics should be used after the identification of the causative organism?

A

N Meningitidis: 2.4g IV benzylpenicillin 4 hourly or chloramphenicol 25mg/kg IV 6 hourly

S Pneumoniae: ceftriaxone or cefotaxime
-add vancomycin if patient is from a penicillin resistant area

H Influenzae: cefotaxime or ceftriaxone

L Monocytogenes: ampicillin 2g 4 hourly + gentamicin 5mg/kg divided into 8 hourly doses

TB: isoniazid + rifampicin + pyrazinamide + pyridoxine

126
Q

What antibiotics should be used in children <3 months and >3 months?

A

< 3 months: cefotaxime plus amoxicillin (to cover listeria contracted during pregnancy)
>3 months: ceftriaxone

127
Q

How else should meningitis be managed?

A

Raised ICP: medical emergency –> manage on ITU w/ mannitol
Seizures: lorazepam IV followed by phenytoin. if seizures continue, treat as status epilepticus
Corticosteroids: IV dexamethasone for 4 days given with initial abx dose

128
Q

What is the post exposure prophylaxis for meningitis?

A

Single dose of ciprofloxacin

129
Q

What is the definition of cauda equina syndrome?

A

The compression of the lumbosacral nerve roots that extend below the spinal cord. Neurosurgical emergency.

130
Q

What are the causes of CES?

A

Lumbar disc herniation (most commonly at L4/5 or L5/S1 level)
Trauma
Spinal tumour
Lumbar spinal stenosis
Epidural abscess or haematoma

131
Q

What are the signs of CES?

A

Bilateral lower limb weakness and/or reduced sensation
Decreased or absent lower limb reflexes
Reduced perianal sensation S2-S4 and reduced anal tone on examination
Palpable bladder due to urinary retention

132
Q

What are the symptoms of CES?

A

Lower back pan and sciatica
Saddle anaesthesia
Bladder and bowel dysfunction –> rarely faecal incontinence, 92% have bladder incontinence
Leg weakness or difficulty walking
Erectile dysfunction

133
Q

What are the investigations for CES?

A

Beside examination eg reflexes, PR exam
MRI w/out IV contrast = GOLD STANDARD. Shows visual lesion and compression of neural structures
Bladder ultrasound: determine if there is urinary retention

134
Q

What is the management for CES?

A

Emergency decompressive laminectomy performed within 24-48 hours of symptom onset
Abx if abscess present

135
Q

What are the complications of CES?

A

Delayed decompression –> permanent leg weakness, sexual dysfunction, urinary dysfunction or chronic pain
Deep vein thrombosis –> high incidence in CES patients
Post op complications –> autonomic dysfunction, recurrent herniation, soft tissue infection or epidural haematoma

136
Q

Define status epilepticus

A

Continuous seizures –> two or more seizures with incomplete recovery in between or a seizure lasting more than 5 minutes. Neurological emergency.

137
Q

What are the causes of status epilepticus?

A

Epilepsy
Febrile illness (kids)
Cerebral infection eg encephalitis or meningitis
Space occupying lesion eg tumour
Subarachnoid haemorrhage
Cerebrovascular disease
Metabolic derangement eg low glucose, low Na, low or high Ca
Drug or alcohol withdrawal
Toxicity eg carbon monoxide

138
Q

What are the investigations for status epilepticus?

A

ECG: arrhythmias can precipitate seizures
ABG/VBG: metabolic acidosis with raised lactate
Metabolic screen eg Na, glucose, Ca
FBCs, U&Es, LFTs
CRP/ESR
Check anti-epileptic drug levels

139
Q

How do you manage status epilepticus?

A

Immediate: A-E assessment, IV access, assess and control airway if needed, continuous monitoring, high flow O2, blood glucose testing

-First give IV diazepam or Lorazepam
-then, if poor nutrition or alcohol abuse IV thiamine
-NOT on phenytoin + seizure duration greater than 10mins: start IV phenytoin
-already on phenytoin + seizure >10mins: IV phenobarbital

Seizure >30mins: GA and transfer to ITU

140
Q

Define trigeminal neuralgia

A

Facial pain syndrome in the distribution of >1 divisions of the trigeminal nerve

141
Q

What are the causes of trigeminal neuralgia?

A

Most common cause: compression of the nerve by a vascular loop near the nerve root entry zone, typically by the superior cerebella artery

-demyelinating disease
-posterior fossa masses
-brainstem infarcts

142
Q

What are the signs of trigeminal neuralgia?

A

Pain provoked by touch w/ attacks lasting less than 1 second up to several hours

143
Q

What are the symptoms of trigeminal neuralgia?

A

Severe facial pain that is trigeminal in distribution, pain tends to be unilateral and electric shock like in sensation, provoked by a trigger eg touch or cold

Some patients experience autonomic symptoms eg lacrimation, facial swelling, rhinorrhoea, ptosis

144
Q

What are the investigations for trigeminal neuralgia?

A

It is a clinical diagnosis

MRI brain to rule out sinister pathology eg tumour or demyelination

145
Q

What is the management for trigeminal neuralgia?

A

Medication:
-1st line: carbamazepine

Surgery:
-microvascular decompression or ablative surgery
-peripheral branch alcohol injection
-cryotherapy

146
Q

What is Wernicke’s encephalopathy?

A

Neurological emergency –> results from thiamine deficiency with varied neurocognitive manifestations

147
Q

What are the risk factors for Wernicke’s encephalopathy?

A

Alcohol abuse
Malnutrition
Anorexia
Malabsorption due to stomach cancer and IBD
Prolonged vomiting eg due to chemotherapy or hyperemesis gravidarum

148
Q

How does alcohol abuse lead to thiamine deficiency (and so Wernicke’s encephalopathy)?

A

Alcohol blocks the phosphorylation of thiamine to its active form thiamine pyrophosphate
Thiamine is normally absorbed in the duodenum. Ethanol prevents the absorption by reducing the gene expression for thiamine transporter 1 within the intestinal brush border
Chronic alcohol abuse can lead to fatty liver or cirrhosis which interferes with the storage of thiamine in the liver

149
Q

How does thiamine deficiency affect the brain?

A

It impairs glucose metabolism and this leads to a decrease in cellular energy –> the brain is vulnerable to this because it uses up so much energy

Cerebellum affected: affects movement and balance
Brain stem affected: motor and sensory innervation to the face and eyes
Medulla region: impair heart rate and breathing

Later stages: haemorrhage and necrosis of the mammillary bodies (responsible for memory, emotion and behaviour)

150
Q

What is Wernicke-Korsakoff syndrome?

A

The combined presence of Wernicke encephalopathy and alcoholic korsakoff syndrome

If Wernicke’s encephalopathy is left untreated, Korsakoff’s psychosis develops in ~80% of patients

151
Q

What are the signs and symptoms of Wernicke’s encephalopathy?

A

Ophthalmoplegia: weakness or paralysis of the eye muscles –> nystagmus, gaze palsies
Ataxia or unsteady gait
Mental state changes –> confusion, apathy and difficulty concentrating

152
Q

What are the signs and symptoms of Wernicke-Korsakoff syndrome?

A

Mainly targets the limbic system
Anterograde amnesia (can’t create new memories)
Retrograde amnesia (inability to recall previous memories)
Confabulation: creating stories to fill in the gaps in their memory which they believe to be true
Behavioural changes

153
Q

What are the investigations for Wernicke’s encephalopathy?

A

Diagnosis is made clinically

Bloods esp LFTs –> measure thiamine levels, blood alcohol levels, liver function may be deranged in alcoholism

CT head: confirm diagnosis by showing degeneration of mammillary bodies

154
Q

How do you manage Wernicke’s encephalopathy?

A

Infusion of thiamine followed by oral supplementation

Usually given alongside glucose of hypoglycaemic (must stabilise thiamine first so as not to induce metabolic acidosis)

Wernicke-Korsakoff is chronic irreversible

155
Q

What are some of the causes of spinal cord compression?

A

Degenerative disc lesions
degenerative vertebral lesions
TB (most common cause of spinal cord compression in countries where TB is endemic)
Epidural abscess
Vertebral neoplasms –> myeloma, metastasis, menningioma, neurofibroma, ependymoma, glioma, lipoma, teratoma
Epidural haemorrhage
Paget’s disease

156
Q

What are general signs of lesion in the spinal cord?

A

Mixed UMN and LMN signs (may also be MND)
Sensory level –> a point at which sensation below that point is abnormal
Sphincter involvement –> a lesion of the spinal cord would cause urinary retention and constipation vs CES causing incontinence
Autonomic dysfunction –> presence of autonomic dysfunction eg HTN, bradycardia, urinary retention, sweating, flushing etc would indicate a lesion above T6

157
Q

How can patients with brain tumours present?

A

Seizure, raised ICP, dementia type symptoms, acute confusional state, stroke –> bleed into the tumour, cranial neuropathies, new onset headache (uncommon to be the presenting complaint for a brain tumour)

158
Q

How are brain tumours classified?

A

Secondary tumours –> most common type of intercranial tumour. Primary sites include lung, breast, bowel and skin

Primary tumours –> divided into parenchymal/intrinsic tumours and most common type of primary brain tumour and extrinsic brain tumours that are surgically separable from the brain

159
Q

What are the usual types of intrinsic brain tumour?

A

Gliomas eg derived from cells of glial origin eg astrocytes and oligodendrocytes
-glioblastoma multiforme is a high grade/grade 4 type of glioma

160
Q

How are extrinsic tumours classified?

A
  1. meningiomas –> arising from the meninges and described in terms of their anatomical location
  2. pituitary adenomas
  3. nerve sheath tumours most commonly vestibular schwannomas (acoustic neuromas)
161
Q

How are brain tumours managed?

A

MRI/CT head to identify tumour plus MRI for interval imaging if the tumour is benign
Surgery
Radiation
-Whole brain and stereotactic radiosurgery are used for secondary tumours
-whole brain and intensity modulated radiotherapy
Chemotherapy: temozolamide is most often used, it is given orally and is an alkylating agent

162
Q

How are brain tumours managed?

A

MRI/CT head to identify tumour plus MRI for interval imaging if the tumour is benign
Surgery
Radiation
-Whole brain and stereotactic radiosurgery are used for secondary tumours
-whole brain and intensity modulated radiotherapy
Chemotherapy: temozolamide is most often used, it is given orally and is an alkylating agent

163
Q

Define acoustic neuroma

A

Benign tumour arising from the schwann cells of the vestibular nerve (also known as vestibular schwannoma)

164
Q

What are the clinical features of acoustic neuroma?

A

Unilateral hearing loss followed by tinnitus, vertigo, unsteady gait, facial numbness and weakness

165
Q

What are the investigations for acoustic neuroma?

A

Audiogram: high frequency hearing loss with speech discrimination worse than expected
CT: usually isointense, enhances with contrast –> expansion of the internal auditory canal
MRI: isointense on T1 and hyperintense on T2 –> may be confined to the internal auditory canal or emerge ‘like an ice cream cone’

166
Q

What is the management for acoustic neuroma?

A

Conservative –> especially if elderly or infirm. Interval MRI imaging to monitor tumour

Surgery:
-excision is curative but high morbidity

Radiotherapy: much lower morbidity compared to surgery and high rate of tumour control

167
Q

Define brain abscess

A

Collection of microbes eg bacterial, fungal, parasitic, within a gliotic capsule occurring within the brain parenchyma

168
Q

What are the risk factors for a brain abscess?

A

-infection of contiguous structures eg dental infection, sinusitis
-skull trauma or surgery
-endocarditis

169
Q

What are the symptoms of a brain abscess?

A

headache
fever
focal neurological deficit eg weakness in extremities
seizures

170
Q

What are the investigations for a brain abscess?

A

Bloods:
-FBC –> elevated WBC
-CRP/ESR elevated
Blood culture: may be positive if cause is bacterial

MRI head with contrast: offers more detail and shows ring enhanced lesions

CT head: less time consuming and cheaper than MRI. Ring enhanced lesions. Less sensitive for early stage abscess and posterior fossa lesions. Ring enhanced lesions.

171
Q

What is the management of brain abscesses?

A

Presumed –> empiric antibiotic therapy eg vancomycin or metronidazole PLUS anti-convulsant for all patients with suspected brain abscess eg phenytoin or carbamazepine or sodium valproate (eg epileptic drugs)

Surgical decompression –> urgent if patients have neurological decompensation
Surgical evacuation –> first line treatment for large >2.5cm lesions and those resistant to medical therapy

Fungal abscess: antifungal eg amphotericin B PLUS anti-convulsant eg carbamazepine

Parasitic abscess: anti-parasitic PLUS anticonvulsant

172
Q

What is Horner Syndrome?

A

A lesion on the sympathetic chain supplying the eye

173
Q

How is Horner’s Syndrome classified?

A

Can be classified according to the site of the lesion alongside the sympathetic chain.
The sympathetic chain involved in Horner’s consists of 3 consecutive neurons which transmits signals from the hypothalamus to the eye
The first and second order neurons are the preganglionic neurons and the third order is the post ganglionic neuron

Differentiate the location of the lesion by the sites affected by anhidrosis:
Anhidrosis of face, arm, trunk = central/first order
Anhidrosis of face= second order
No anhidrosis= third order

174
Q

What is first order (central) Horner’s?

A

The first order neurons span from the hypothalamus to the T1 spinal cord segment

These lesions often arise from MS or brain tumours
Strokes can also cause central Horner’s and present with other cranial nerve palsies –> most common stroke syndrome is Wallenberg’s (lateral medullary) syndrome

175
Q

What is second order Horner’s?

A

The second order neuron leaves the spinal cord and travels towards the head via the cervical sympathetic chain and terminates at the superior cervical ganglion. It exits the spinal cord near the upper lobe of the lung

Causes included pancoast tumours (apical lung cancer), thyroid malignancy, iatrogenic and traumatic causes

176
Q

What is third order (post ganglionic) Horner’s?

A

The third order neuron arises from the superior cervical ganglion and travels alongside the internal carotid artery to the cavernous sinus where the sympathetic fibres join the ophthalmic nerve.

Causes of post ganglionic lesions include carotid artery dissection, cavernous sinus thrombosis and rarely cluster headaches

177
Q

What is the Horner’s Syndrome triad?

A

Ptosis
Anhidrosis
Miosis (constricted pupil)

On the ipsilateral side

178
Q

What are the investigations for Horner’s Syndrome?

A

Clinically –> presence if systemic features with Horner’s eg patient’s with cough and weight lost may have a Pancoast tumour

Eye drops –> apraclonidine eye drops are put in the eye and reverse the pupillary constriction
-hydroxyamphetamine drops an identify the location of lesion –> it will dilate a constricted Horner’s pupil if there is an underlying preganglionic lesion

179
Q

What is the management of Horner’s syndrome?

A

Depends on the underlying cause

180
Q

What is Ramsay Hunt syndrome?

A

a facial nerve palsy caused by shingles of the facial nerve

181
Q

What is Bell’s Palsy?

A

Also known as facial nerve palsy –> isolated dysfunction of the facial nerve that typically presents with unilateral facial weakness. It is a unilateral LMN facial palsy.

182
Q

What are the five branches of the facial nerve?

A

Temporal
Zygomatic
Buccal
Marginal mandibular
Cervical

183
Q

What is the motor function of the facial nerve?

A

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

184
Q

What is the sensory function of the facial nerve?

A

carries taste from the anterior 2/3 of the tongue

185
Q

What is the parasympathetic function of the facial nerve?

A

supply to the submandibular & sublingual salivary glands and the lacrimal gland

186
Q

How do you distinguish between an upper motor neurone and lower motor neurone?

A

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

Therefore: in an UMN lesion, the forehead will be spared and the patient can move their forehead on the affected side. In a LMN lesion, the forehead will not be spared and they won’t be able to move their forehead on the affected side

187
Q

What can cause unilateral UMN lesions?

A

Strokes
Tumours

188
Q

What are the signs and symptoms of Bell’s Palsy?

A

rapid onset unilateral facial nerve weakness
generalised weakness of the affected side –> patient unable to show teeth, screw up eye and raise eyebrows on affected side
may not be able to fully close eyes –> will need lubricating eye drops

189
Q

What is the scale sometimes used in Bell’s Palsy called?

A

House-Brackman: sometimes used to describe the degree of paralysis

190
Q

What is the treatment for Bell’s Palsy?

A

Steroids: prednisolone if given with 72 hours of onset
Anti virals: aciclovir as many cases are caused by herpes or zoster
Eye care if struggling to close eyes

191
Q

What is bulbar palsy?

A

Lesions in the motor nuclei of the medulla. It consists of LMN signs in regions innervated by the facial, glossopharyngeal, vagus and hypoglossal nerves

192
Q

What are the signs and symptoms of a bulbar palsy?

A

Palsy of the tongue, facial muscles and swallowing
Signs appear like LMN signs eg flaccid, fasciculating tongue
Jaw jerk is normal
Speech may be quiet, hoarse or nasal

193
Q

What are the causes of bulbar palsy?

A

MND
Guillain-Barre syndrome
Polio
Syringobulbia
Brainstem
Myasthenia gravis
Myotonic dystrophy

194
Q

What is cerebral palsy?

A

A movement disorder that results from a non progressive lesion of motor pathways. Specific symptoms will depend on where the lesion is & can affect any part of the brain eg cerebellar, basal ganglia, cerebral

195
Q

What are the causes of cerebral palsy?

A

Antenatal causes: gene deletions, antenatal infection, vascular occlusion, failure of cortical migration
Hypoxic ischaemic brain injury
Post natal causes: pre term babies are at increased risk, head injury, meningitis, encephalitis, encephalopathy, hypoglycaemia, hydrocephalus, hyperbilirubinaemia

196
Q

What are the signs and symptoms of cerebral palsy?

A

May be present at birth but commonly seen in infancy as motor milestones may be missed, but sometimes diagnosis can be delayed or missed into early childhood eg 6yo

Floppy baby –> reduced muscle tone in the neonate
Increased tone –> seen in older children consistent with UMN lesion
Feeding difficulties
Delayed motor milestones eg late walker or crawler
Asymmetric hand movement eg hand preference before 12 months old
Persistence of primitive reflexed eg moro or stepping reflex

197
Q

What are the 4 patterns of symptoms in cerebral palsy?

A

Spastic: lesion is in the pyramidal or corticospinal tract
Dystonic: lesion is in the basal ganglia
Ataxic: cerebellum
Mixed

198
Q

What are the signs and symptoms of spastic cerebral palsy?

A

UMN lesions in corticospinal or pyramidal tract with UMN signs eg brisk reflexes, spasticity, extensor plantar response

199
Q

What are the types of cerebral palsy?

A

Hemiplegic
Quadriplegic
Diplegic

200
Q

What are the signs and symptoms of ataxic hypotonic cerebral palsy?

A

typically symmetrical
hypotonia, poor balance and delayed motor development
uncoordinated movements
tremor

201
Q

Describe dyskinetic cerebral palsy?

A

Dyskinesia: fluctuating muscle tone giving rise to involuntary limb movements
Usually affects all 4 limbs
types of involuntary movement include chorea, dystonia and athetosis (involvement of the distal limbs)

202
Q

What is the management of cerebral palsy?

A

No curative treatment
Once a child is diagnosed their care is by an MDT known as the CDS (child development services)
Specific management includes:
-physiotherapy of affected limbs
-splinting of affected contractured joints
-botox injections into spastic muscles
-speech & language therapy

203
Q

What is peripheral neuropathy?

A

a broad term that refers to any disorder of the peripheral nerves that make up the peripheral nervous system

204
Q

What are the different types of peripheral neuropathies and what do they affect?

A

Radiculopathies: involvement of a spinal nerve root
Polyneuropathies: generalised involvement of multiple peripheral nerves
Mononeuropathy: involvement of a single nerve

205
Q

What are the different types of peripheral neuropathies and what do they affect?

A

Radiculopathies: involvement of a spinal nerve root
Polyneuropathies: generalised involvement of multiple peripheral nerves
Mononeuropathy: involvement of a single nerve

206
Q

What are the causes of peripheral neuropathies?

A

D-diabetes
A-alcoholism
V-vitamin deficiency B12
I-infective/Inherited eg GBS or charcot marie tooth
D-drugs eg isoniazid

207
Q

Describe the six main mechanisms of peripheral nerve degeneration?

A

1: demyelination eg GBS as a result of schwann cell damage
2: axonal degeneration. usually occurs in toxic neuropathies where conduction speed remains normal and the axon dies peripherally first.
3: wallerian degeneration: fibre degeneration when the fibre is cut or crushed –> both the axon and the myelin sheath will degenerate over several weeks after the incident
4: compression eg carpal tunnel syndrome where here is local demyelination at the site of compression
5: infarction there will also be wallerian degeneration distal to the infarct
6: infiltration eg leprosy, malignancy, inflammation or sarcoidosis

208
Q

What are the different types of neuropathy in diabetes?

A

symmetrical, mainly sensory neuropathy in distal regions
acute painful neuropathy
mononeuropathy or mononeuritis multiplex
diabetic amyotrophy
autonomic neuropathy

209
Q

What are 4 parasites that can causes malaria in humans?

A

P. falciparum
P. vivax
P. ovale
P. malariae

210
Q

How is malaria transmitted?

A

by the bite of a female anopheline mosquito
can also be acquired transplacentaly, by transfusion or innoculation

211
Q

What are the signs and symptoms of malaria?

A

Signs: pallor (due to anaemia), jaundice (due to unconjugated bilirubin from destruction of RBCs), hepatosplenomegaly (due to compensation for anaemia)

Symptoms: fever, sweats, rigors, fatigue, headache, myalgia, vomiting

212
Q

What are the investigations for malaria?

A

Malaria blood film: will show the parasites, the concentration and also what type they are
FBC, U&E, LFTs: thrombocytopenia, elevated lactate dehydrogenase levels due to haemolysis and normochromic/normocytic anaemia

213
Q

What is the management of malaria?

A

Uncomplicated Malaria: oral artemether with lumefantrine (riamet) OR proguanil & quinine sulphate (malarone) OR quinine (quinine has become old fashioned as some parasites are now resistant to it)

Complicated malaria:
IV artesunate (most effective)
IV quinine dihydrochloride

214
Q

What is shingles?

A

a temporary self limiting illness characterised by a painful rash caused by the herpes zoster (varicella zoster) virus specifically human herpesvirus-3 eg HHV 3

215
Q

How does shingles occur?

A

Primary infection with HHV3/varicella zoster causes chicken pox that can be subclinical
After primary infection, the virus lies dormant in the CNS in the root ganglia either the dorsal root ganglia, the trigeminal ganglion or the facial nerve (geniculate) ganglion
An episode of shingles occurs when the virus reactivates and travels down the nerve, causing inflammation along the nerve itself with pain and rash in a dermatomal pattern

216
Q

What are the clinical features of shingles?

A

Critical feature of a shingles rash is the dermatomal distribution (it NEVER crosses the midline)
-pain: usually the first symptom & may be associated with paraesthesia in the skin
-rash: vesicular herpetic rash, fluid filled vesicles in the clusters typically appearing 1-3 days after the onset of pain, accompanied with itching and burning

Symptoms last 2-3 weeks in younger patients and longer in older patients
Post herpetic neuralgia is a common complication

217
Q

What sites are commonly affected by shingles?

A

lower thoracic region (most commonly)
ophthalmic division of the trigeminal nerve
occasionally motor nerves causing paralysis eg facial paralysis in Ramsay Hunt syndrome

218
Q

What are the investigations for shingles?

A

Usually a clinical diagnosis
If in doubt –> a viral/PCR swab can be sent of skin lesions to confirm diagnosis

219
Q

What is the management of shingles?

A

keep rash clean, dry and covered –> if effectively covered, risk of transmission is low
Rash is no longer infectious once all the lesions have dried
Topical therapies not recommended
Oral antiviral therapy eg aciclovir

220
Q

What are the complications of shingles?

A

post herpetic neuralgia
herpes zoster ophthalmicus

221
Q

What is Meniere’s disease?

A

a long term inner ear disorder that causes recurrent attacks of vertigo. It is associated with the excessive build up of endolymph in the labyrinth of the inner ear causing higher pressure than normal and disrupting sensory signals (this increased pressure of the endolymph is called endolymphatic hydrops)

222
Q

What are the signs and symptoms of Meniere’s disease?

A

Typically in a patient 40-50 years old
Unilateral episodes of vertigo, hearing loss and tinnitus (common triad tested in exams)
-the vertigo comes in episodes of 20 mins - 1hour coming in clusters over several weeks followed by prolonged periods without vertigo
-hearing loss fluctuates at first & is associated with vertigo attacks before gradually becoming more permanent, affecting low frequencies first
-tinnitus initially occurs with episodes of vertigo before eventually becoming permanent

May also have sensation of fullness in the ear, unexplained falls without loss of consciousness & imbalance

223
Q

What are the signs and symptoms of Meniere’s disease?

A

Typically in a patient 40-50 years old
Unilateral episodes of vertigo, hearing loss and tinnitus (common triad tested in exams)
-the vertigo comes in episodes of 20 mins - 1hour coming in clusters over several weeks followed by prolonged periods without vertigo
-hearing loss fluctuates at first & is associated with vertigo attacks before gradually becoming more permanent, affecting low frequencies first
-tinnitus initially occurs with episodes of vertigo before eventually becoming permanent

May also have sensation of fullness in the ear, unexplained falls without loss of consciousness & imbalance

224
Q

What are the investigations for Meniere’s disease?

A

normally a clinical diagnosis by an ENT specialist
audiology assessment –> low frequency hearing loss

225
Q

What is the management of Meniere’s disease?

A

acute attacks: prochloperazine or antihistamines eg cyclizine
prophylaxis: betahistine

reduce sodium intake and consider thiazide diuretics eg bendroflumethiazide
Surgical options: endolymphatic sac surgery & intercranial vestibular nerve section

226
Q

What is benign essential tremor?

A

common condition associated with older age characterised by a fine tremor affecting all voluntary muscles

227
Q

What are the features of an essential tremor?

A

fine tremor
symmetrical
more prominent on voluntary movement
never involves legs
absent during sleep
improved by alcohol

228
Q

What is the management of essential tremor?

A

propranolol
primidone (an anti-epileptic)

229
Q

What is neurofibromatosis?

A

a genetic condition that causes neuromas to develop through the nervous system –> the tumours are benign. There are two types: NF1 and NF2 with NF1 being the more common one

230
Q

How is NF1 inherited?

A

autosomal dominant inheritance
gene on chromosome 17 –> codes for neurofibrin which is a tumour suppressor protein

231
Q

What is the diagnostic criteria for NF1?

A

Must be at least 2 of the 7 features
(remember with pneumonic CRABBING)
C: cafe au lait spots measuring >5mm in children and >15mm in adults
R: 1st degree relative with NF1
A: axillary or inguinal freckles
BB: bony dysplasia eg Bowing of the long bone or sphenoid wing dysplasia
I: iris hamartomas (Lisch nodules) - yellow or brown lesions on the iris
N: neurofibromas (2 or more) or 1 plexiform neurofibroma
G: glioma of the optic nerve

232
Q

What are the investigations for NF1?

A

diagnosis is based on clinical criteria
genetic testing if in doubt
imaging of lesions or bones if needed

233
Q

What is the management of NF1?

A

no curative treatment –> symptomatic neurofibromas are often removed
genetic counselling to all patients when considering having a family

234
Q

What is the inheritance of NF2?

A

autosomal dominant
gene on chromosome 22 –> codes for merlin which is a tumour suppressor protein associated with schwann cells

235
Q

How is a diagnosis of NF2 made?

A

If either of the following are present:
-bilateral vestibular schwannomas (presenting as bilateral sensorineural hearing loss in patients <30) the schwannomas are actually a form of acoustic neuroma
-1st degree relative with NF2 AND either

unilateral vestibular schwannoma or one of –>
-neurofibroma
-meningioma
-glioma
juvenile cataract

EXAM TIP: bilateral acoustic neuromas almost certainly indicate NF2

236
Q

What is the management of NF2?

A

survival from diagnosis –> typically 15 years
no curative treatment
management based around screening in at risk patients –> annual hearing tests are a useful screening tool
surgery –> to remove schwannomas
no disease present at 20 on an MRI implies low risk
if no disease present at 30 on MRI can almost guarantee the gene hasn’t been inherited (except when there is a fhx of late onset disease)

237
Q

Define muscular dystrophy

A

An umbrella term for genetic conditions that cause gradual weakening and wasting of the muscles

238
Q

List some of the types of muscular dystrophy

A

Duchennes
Beckers
Myotonic
Facioscapulohumeral
Oculopharyngeal

239
Q

What is Gower’s sign?

A

Seen in children with proximal muscle weakness when they stand up from a lying position –> use their hands on their legs to help them stand up

240
Q

What is Duchennes muscular dystrophy?

A

Most common type of MD. Caused by defective gene for dystrophin on X chromosome. Inheritance is X linked recessive

241
Q

What are the signs and symptoms of Duchennes muscular dystrophy?

A

Trouble getting up from a chair
Trouble getting upstairs
Clumsiness
Waddling gait
General difficulty with motor skills
Skeletal deformity
Wasting of proximal muscles & calf swelling due to pseudohypertrophy
Positive Gower’s test

242
Q

What are the investigations for Duchennes?

A

Positive Gower’s test
Increased levels of creatinine kinase in the blood
EMG –> shows destruction of muscle tissue rather than issues with nerve conduction
Genetic testing will show Xp21 defect
Muscle biopsy –> shows an absence of dystrophin

243
Q

How is Duchennes managed?

A

Corticosteroids –> aggressively used can have good outcome and prolong life expectancy
Physiotherapy
Mechanical ventilation –> required in later stages

244
Q

What is Beckers muscular dystrophy?

A

The same gene as in Duchennes is affected however the dystrophin gene is less severely affected and maintains some of its function. management and investigations are similar to duchennes.

245
Q

What is Myotonic Dystrophy?

A

Another type of muscular dystrophy caused by a different gene. Features include progressive muscle weakness, prolonged muscle contractions, cataracts & cardiac arrhythmias

Exam tip –> may present in exams as someone being unable to let go after shaking someone’s hand/trouble letting go of a door handle

246
Q

What is hydrocephalus?

A

The build up of CSF within the brain and spinal cord. Is either a result of over production of CSF or a problem draining or absorbing CSF.

247
Q

Describe normal CSF physiology

A

The four brain ventricles contain the CSF which provides a cushion for the brain tissue. CSF is created in the 4 choroid plexuses (one in each ventricle) and by the walls of the ventricles. CSF is absorbed into the venous system by the arachnoid granulations.

248
Q

What are the causes of hydrocephalus?

A
  • Aqueductal stenosis (congenital) –> when the cerebral aqueduct that connects the third and fourth ventricles is narrowed. This blocks the normal flow of CSF out of the third ventricle, causing CSF to build up in the lateral and third ventricles
  • arachnoid cysts can block the outflow of CSF if they are large enough
  • Arnold-chiari malformation where the cerebellum herniates downwards through the foramen magnum and blocks the outflow of CSF
  • chromosomal/other congenital malformations
249
Q

What are the signs and symptoms of hydrocephalus?

A

Baby –> enlarged and rapidly increasing head circumference
-bulging anterior fontanelle
-poor feeding and vomiting
-poor tone
-sleepiness

250
Q

What are the signs and symptoms of hydrocephalus?

A

Baby –> enlarged and rapidly increasing head circumference
-bulging anterior fontanelle
-poor feeding and vomiting
-poor tone
-sleepiness

251
Q

What is the treatment for hydrocephalus?

A

Ventriculoperitoneal shunt –> drains CSF from the ventricles into another body cavity, usually the peritoneal

252
Q

Define radiculopathy

A

Compression of a nerve root in the spinal column
–> impact on motor axons causes weakness & impact on sensory axons causing anaesthesia/paraesthesia

253
Q

What is the most common cause of radiculopathy?

A

nerve compression

254
Q

What are the causes of nerve compression?

A

Intervertebral disc prolapse –> lumbar spine most vulnerable to this
Degenerative diseases of the spine
Fracture
Malignancy
Infection eg osteomyelitis

255
Q

What are the signs and symptoms of radiculopathy?

A

numbness, tingling & weakness
radicular pain –> burning/deep/narrow

redflags –> faecal incontinence, urinary retention, saddle anaesthesia (CAUDA EQUINA SYNDROME)

256
Q

What is the management of radiculopathy?

A

Depends on cause –> treat cause eg surgical treatment of CES
Analgesia
Amitriptyline or gabapentin
Physiotherapy

257
Q

What is narcolepsy?

A

Rare. Brain loses the ability to regulate the sleep wake cycle, leading to excessive day time sleepiness and REM abnormalities.

258
Q

What is narcolepsy?

A

Rare. Brain loses the ability to regulate the sleep wake cycle, leading to excessive day time sleepiness and REM abnormalities.

259
Q

What is the cause of narcolepsy?

A

Orexin (hypocretin) is a neurotransmitter involved in sleep. Loss of orexin secreting neurons in the hypothalamus results in narcolepsy. Most cases are thought to be autoimmune related. Strong genetic association with HLA subtypes.

260
Q

What are the signs and symptoms of narcolepsy?

A

Excessive day time sleepiness with no other clear cause
Disrupted nighttime sleep/vivid dreams
Cataplexy –> conscious collapse caused by muscle atonia, often in response to sudden emotion
Hypnagogic/hypnopompic hallucinations –> dream like hallucinations at the point of emerging from/entering REM sleep
Sleep paralysis

261
Q

Define Parkinson’s Disease

A

Progressive reduction in dopamine in the basal ganglia of the brain, leading to movement disorder.

262
Q

Describe the pathology of Parkinson’s?

A

Results from the loss of dopaminergic neurons in the basal ganglia → mostly the substantia nigra
Surviving neurons contain aggregations of proteins → alpha synuclein (Lewy Bodies).

263
Q

RF for Parkinson’s?

A

FHx
Previous head injury
Pesticides
HIV
Encephalitis

264
Q

Protective factors for Parkinson’s?

A

Smoking
Caffeine
Physical activity

265
Q

Presentation of Parkinson’s?

A

Unilateral tremor: more pronounced when resting and improves on voluntary movement
Cogwheel rigidity: resistance to passive movement of the joint
Bradykinesia: handwriting gets smaller, shuffling gait, difficulty initiating movement, difficulty turning around, reduced facial movements & facial expressions

Other features: depression, sleep disturbance, anosmia, postural instability, cognitive impairment & memory problems

266
Q

Parkinson’s vs BET

A

Parkinson’s: asymmetrical tremor, 4-6Hz, worse at rest, improves with intentional movement, no change with alcohol

BET: symmetrical, 5-8Hz, improves at rest, worse with intentional movement, improves with alcohol

267
Q

Other causes of Parkinsonism?

A

Drug Induced: anti-psychotics eg clozapine, risperidone, anti-emetics eg metoclopramide
CVD eg repeated strokes
Non-Parkinson’s dementia eg Lewy Body dementia
Progressive supranuclear palsy
Multiple system atrophy
Wilson’s Disease

268
Q

Management of Parkinson’s?

A

referral to neurologist

Levodopa: synthetic dopamine, combined with a drug to stop it getting broken down before it reaches the brain (peripheral decarboxylase inhibitors→ co-benyldopa (levodopa & benserazide). Becomes less effective over time & usually used when other treatments not working

COMT inhibitors: entacapone. Metabolises levodopa in brain & body. Taken with levodopa to extend effective duration of it.

Dopamine Agonists: mimic dopamine in the basal ganglia & stimulate the dopamine receptors. Ropinirole or Cabergoline

Monoamine Oxidase B inhibitors: block enzymes from breaking down circulating dopamine. Selegiline or Rasagiline

269
Q

Nausea medication in Parkinson’s?

A

Domperidone

270
Q

Which drugs to avoid in Parkinson’s?

A

Haloperidol, Metoclopramide, Cyclizine (any drugs that have a side effect of Parkinsonism)

271
Q

Main side effect of too much dopamine?

A

Dyskinesias →

Dystonia: excessive muscle contraction
Chorea: abnormal involuntary movements that can be jerking or random
Athetosis: involuntary twisting or writing movements

272
Q

CN III palsy?

A

Oculomotor. Most CN palsies are one sided.

Down & out gaze (exotropia)
Ptosis
Double vision
Pupils affected (ONLY if outer nerve fibres affected)

273
Q

CN IV palsy?

A

Trochlear nerve. Controls the superior oblique muscle.

Vertical Double vision
Turning up of affected eye
Inability to gaze down/inwards (so difficulty going downstairs/doing things that require you to look down)

274
Q

CN VI palsy?

A

Abducens. Controls the lateral rectus muscle.

Horizontal double vision
Affected eye drifts towards the nose
May also have hearing issues, facial weakness & numbness

275
Q

UMN vs LMN signs?

A

UMN: spasticity, hyperreflexia, ankle clonus, positive Babinski

LMN: Flaccid, hyporeflexia/absent, fasciculations

276
Q

How is GCS calculated?

A

Eye opening (out of 4):
4: spontaneously
3: to speech
2: to pain
1: no response

Verbal response out of 5):
5: orientated
4: confused
3: words
2: sounds
1: nothing

Motor response (out of 6)
6: obeys command
5: localise to pain
4: normal flexion
3: abnormal flexion
2: extension
1: nothing

277
Q

How to use GCS to guide management?

A

8 = intubate

CT within 1 hour if GCS <13 @ presentation, GCS <15 after 2 hours or fracture, panda eyes, battle sign, seizure, >1 episode of vomiting

CT within 8 hours if:
>65 years, bleeding or clotting disorder, dangerous mechanism of injury or >30 mins retrograde amnesia

278
Q

What is NPH?

A

Reversible cause of dementia seen in elderly patients

279
Q

Causes of NPH?

A

Secondary to head injury, subarachnoid haemorrhage, meningitis

280
Q

Signs & Symptoms of NPH?

A

Triad: dementia, gait abnormality, urinary incontinence

281
Q

Investigations for NPH?

A

CT head: ventriculomegaly in the absence/out of proportion to sulcal enlargement

282
Q

Management for NPH?

A

VP shunt

Phase 3a (8 decks)

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