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EOY4 > Neurology > Flashcards

Neurology Flashcards

1
Q

What is the location of a Lumbar Puncture?

A

Between L3 and L4

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2
Q

What is the function of the Cerebellum?

A

Control of motor function and maintenance of muscle tone

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3
Q

What are the 3 functional and anatomical divisions of the cerebellum?

A

Cerebrocerebellum - Planning movements, motor learning and coordination of muscle activation

Spinocerebellum (vermis + intermediate zone) - Body movements and receives proprioceptive information

Vestibulocerebellum (flocculonodular) - Balance control and ocular reflexes e.g. fixation on a target. Receives input from the vestibular system.

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4
Q

What is the blood supply to the cerebellum?

A

Superior Cerebellar Artery (SCA) and Anterior Inferior Cerebral Artery (AICA) from BASILAR ARTERY

Posterior Inferior Cerebellar Artery (PICA) from VERTEBRAL ARTERY

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5
Q

What are the causes of cerebellar dysfunction? (PASTRIES)

A 
Posterior fossa tumour
Alcohol misuse
Stroke
Trauma
Rare causes
Inherited - Friedrich’s Ataxia
Epilepsy medications
Sclerosis (MS)
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6
Q

What are the symptoms of cerebellar dysfunction? (DANISH)

A

Dysdiadochokinesia and Dysmetria

Ataxic gait

Nystagmus

Intention tremor

Slurred speech

Hypotonia

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7
Q

What is dysdiadochokinesia and what is dysmetria?

A

Dysdiadochokinesia = impaired rapidly alternating movements

Dysmetria = past pointing

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8
Q

Which part of the cerebellum is damaged to give dysdiadochokinesia, dysmetria, ataxic gait and intention tremor?

A

Spinocerebellum

Basilar infarct/ SCA/ AICA

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9
Q

Which part of the cerebellum is damaged to give Nystagmus?

A

Vestibulocerebellum

PICA infarct

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10
Q

Are cerebellar signs contralateral or ipsilateral and why?

A

Ipsilateral

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11
Q

What is the function of the basal ganglia?

A

Regulation of movement by providing a feedback mechanism to the cerebral cortex

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12
Q

Where is the basal ganglia located?

A

Forebrain and midbrain

Part of the extrapyramidal system

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13
Q

How does the extrapyramidal system differ to the corticospinal tracts?

A

Involuntary actions whereas corticospinal is voluntary

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14
Q

What is the direct pathway?

A

Excitatory

Excitation of the striatum = ↑ inhibition of the Globus Pallidus Interna and Substantia Nigra

↓ inhibition of the Thalamus (as GPi and SNR inhibit thalamus) = ↑ excitation of the motor cortex

Movement!

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15
Q

What is the indirect pathway?

A

Inhibitory

Excitation of the striatum = ↑ inhibition of the Globus Pallidus Externa

↓ inhibition of the Subthalamic nucleus (as GPe inhibits STN)

↑ excitation of the Substantia Nigra (as STN excites)

↑ inhibition of the Thalamus (as SNR inhibits) = ↓ excitation of the motor cortex

↓ movement

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16
Q

What is the function of the direct and indirect pathways?

A

Regulation between the two pathways is what allows control and coordination of movement

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17
Q

What is the pathophysiology behind Parkinson’s disease?

A

The degradation of dopaminergic neurones in the Substantia Nigra Pars Compacta

Lewy bodies are also present in the basal ganglia, brain stem and cortex

Leads to dysregulation between the direct and indirect pathways

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18
Q

What is the Parkinsonism triad?

A

Resting tremor - pill rolling

Hypertonia - Cogwheel Rigidity (hypertonia + tremor)
No muscle weakness

Bradykinesia

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19
Q

How does bradykinesia present in PD?

A

Slow to start moving

Slow actions that decrease in amplitude upon repetition e.g. Micrographia

Festinant gait (shuffling, forward leaning)

Might stop in doorways

Reduced facial expressions

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20
Q

What are the autonomic effects of PD?

A

Postural hypotension
Constipation
Dribbling

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21
Q

What are the neuropsychiatric effects of PD?

A

Depression

Psychosis

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22
Q

How is PD mainly diagnosed?

A

Clinical diagnosis

Triad is progressive and signs are usually worse on one side

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23
Q

Which drugs must be excluded when diagnosing PD?

A

Psychiatric drugs - typical antipsychotics/ methyldopa/ memantine

Anti-emetics e.g. metoclopramide

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24
Q

Which other conditions must be excluded when diagnosing PD?

A

Wilson’s disease

Non-Parkinson’s dementias e.g. Dementia with Lewy Bodies, Frontotemporal dementia

Other tremor causes e.g. essential Tremor

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25
Q

What is the conservative management of PD?

A

Refer to neurologist/stop the drug causing the Parkinsonism

Provide patient and family with written info and support sources e.g. a leaflet and Parkinson’s UK

Inform DVLA

MDT involvement

Manage other symptoms as and when e.g. constipation, sleep disturbance

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26
Q

What is the medical management of PD?

A

1) Levodopa + Co-Beneldopa - Dopamine precursor + Dopa Decarboxylase Inhibitor.
2) MAO-B inhibitor e,g. Selegiline
3) Oral Dopamine Agonists e.g. Pramiprexole

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27
Q

What is the MOA of Levodopa + Co-Beneldopa

A

Dopamine precursor + Dopa Decarboxylase Inhibitor.

Dopamine can cross through the blood brain barrier but DCI cannot.

This prevents the synthesis of dopamine in the peripheries therefore reducing adverse side effects!

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28
Q

What are the side effects of Levodopa + Co-Beneldopa

A 
dyskinesia
painful dystonia
psychosis
visual hallucinations
N&V
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29
Q

What are the side effects of MAO-B inhibitor

A

Don’t worry about tyrosine rich food (MAO-A).

Side effects = atrial fibrillation and postural hypotension

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30
Q

What are the adjuvant medical treatments for PD?

A

COMT - catechol-O-methyl transferase (COMT) inhibitors. Prevents methylation of dopamine and levodopa (LFT monitoring)

Amantadine - actually an antiviral! ↑ exogenous dopamine production (not much evidence)

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31
Q

What must be considered with the medical management of PD?

A

Efficacy reduces over time

Can’t withdraw suddenly due to risk of neuroleptic malignant syndrome and acute akinesia (careful if vomiting or something)

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32
Q

What is the surgical management of PD? When would this be considered?

A

Deep brain stimulation

Motor complications that are refractory to medical treatment

dopamine responsive

no co-morbid mental health conditions

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33
Q

What is Multiple Sclerosis?

A

Chronic and progressive demyelination of nerves found in the central nervous system and spinal cord.

Never affects peripheral nerves.

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34
Q

What is the pathophysiology of MS? (big card)

A

T cell (CD4 helper and CD8 cytotoxic) mediated degradation of the myelin sheaths

Myelin activates T cells then BBB expresses specific receptors to allow more T cells in and cause further damage

TNF-a and Interleukins also increase permeability of the BBB and allow more T cells in

This attracts B cells and macrophages which attack the Oligodendrocytes

- Prevents further production of myelin
- Scar tissue formation = plaques on oligodendrocytes

Remyelination initially occurs but eventually stops - relapses?

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35
Q

What type of hypersensitivity reaction is MS?

A

Type 4!

ABCDDDDD - takes days

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36
Q

What are the 4 types of MS?

A

Relapsing and remitting - most common + periods of attacks

Primary Progressive - 1 constant attack

Secondary Progressive - Starts as relapsing and remitting but becomes progressive

Progressive Relapsing - Bouts of attacks but getting worse overall

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37
Q

What are the non-modifiable risk factors for MS?

A

Female

Genetics - HLA-DR2 gene

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38
Q

What are the modifiable risk factors for MS?

A

Infections (+genetic vulnerability) - EBV and Herpes 6 (Roseola Infantum)

Vitamin D Deficiency

Smoking

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39
Q

How does MS commonly present?

A

Optic nerve affected = Optic Neuritis

brainstem affected = nystagmus and diplopia

other motor deficits e.g. spasticity/ataxia/dysarthria/intention tremor

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40
Q

What is optic neuritis?

A

Sudden blurred vision and unilateral eye pain

loss of visual acuity (hole in the middle) and contrast sensitivity (red in particular)

Get a relative afferent pupillary defect (see opthalmology)

Swelling of optic disc margins but not papilloedema

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41
Q

How can MS present as sensory symptoms?

A

Pain and loss of sensation

Lhermitte’s sign (sudden sensation resembling an electric shock that passes down the back of your neck and into your spine and may then radiate out into your arms and legs)

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42
Q

What are other symptoms of MS?

A

Autonomic System
Bladder, bowel and sexual dysfunction

Cognitive System
Later

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43
Q

What are 2x Ddx for MS?

A

Systemic Inflammatory Disease e.g. SLE, Sarcoidosis (won’t have Antibody in CSF)

Space Occupying Lesions e.g. vascular

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44
Q

How is MS diagnosed?

A

MRI of brain and spinal cord is definitive

Lumbar Puncture

Nerve conduction studies (lower amplitude)

+ absence of other treatable causes

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45
Q

What is the conservative treatment for MS?

A

R&R

Physical and psychological support, occupational therapy

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46
Q

What is the medical management for MS?

A

Corticosteroids (IM Methylprednisolone)
IVIG
Plasmapheresis
Immunosuppressants

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47
Q

Which immunosuppressants are used for MS?

A

Immunomodulating - B-Interferons to reduced inflammation and maintain BBB

Glativamer Acetate - Similar antigens to myelin so T cells compete

Monoclonal antibodies - lots of side effects e.g. increased risk of progressive multifocal leucoencphalopathy due to JC virus. PML = lytic infection of oligodendrocytes AND cancer

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48
Q

What is Guillan Barre Syndrome?

A

Inflammatory, demyelinating polyneuritis causing muscle weakness and loss of sensation

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49
Q

How does GBS normally present?

A

Elderly

Sudden onset paralysis

Starts at feet and ascends with a variable rate of progression
Max. Weakness usually at 2-3 weeks
Bilateral
Back, shoulder and thigh pain
Associated parasthesia, numbness and absent deep tendon reflexes

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50
Q

What are the required features to diagnose GBS?

A

Bilateral progressive weakness in the upper and lower limbs

Hyporeflexia

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51
Q

What are the 2 most serious complications of GBS?

A

Weakness eventually reaches the respiratory muscles = respiratory failure type 2

Autonomic dysfunction so urinary retention etc

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52
Q

What are some other complications of GBS? (5)

A 
Pain
VTE
SIADH
Renal Failure (following IVIG)
Immobility = VTE and Hypercalcaemia
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53
Q

What is the natural progression of GBS?

A

Often following an infection. Usually 1-3 weeks after

Campylobacter Jejuni (gastroenteritis)

Cytomegalovirus

Epstein-Barr Virus

Mycoplasma Pneumoniae

Flu vaccine may be associated (???)

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54
Q

What are the 4 sub types of GBS?

A

Acute Inflammatory Demyelinating Polyradiculoneuropathy (most common)

Acute Motor Axonal Neuropathy

Acute Motor and Sensory Axonal Neuropathy

Acute Pandysautonomia

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55
Q

What are the main investigations for GBS?

A

Mainly a clinical diagnosis. Do bedside spirometry to monitor FVC!!!

BUT can do a lumbar puncture and look for proteins in the CSF to exclude Polio and Lymphoma

Nerve conduction studies to exclude other causes of muscle weakness

Campylobacter Serology if GI upset - AMAN = anti GM1

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56
Q

What is the treatment of GBS?

A

General Supportive Management

IVIG

Plasmapheresis within the first 2 weeks of onset

Not steroids as they may worsen symptoms!

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57
Q

What is the neuromuscular junction?

A

The synapse between a motor neurone and its corresponding muscle fibre

The muscular end plate has lots of junctional folds in which ligand gated (Acetylcholine) ion channels sit

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58
Q

Which ion channels are located on the muscular end plates?

A

Nicotinic (ionotropic so have integral ion channel. For short and rapid responses.)

or Muscarinic (metabotropic so GPCR and longer response)

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59
Q

Which enzyme is present on the muscular end plate and why?

A

Acetylcholinesterase is also present on the end plate to terminate the effect following contraction.

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60
Q

What is myasthenia gravis?

A

Autoimmune condition

B cells make an antibody that blocks the Nicotinic Acetylcholine Receptor on the muscular end plate

Deficient/reduced Acetylcholine means that the muscle can’t contract = weakness

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61
Q

What type of hypersensitivity reaction is myasthenia gravis?

A

ABBBBBBCD = B

Type 2! B cells involved

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62
Q

What are the main symptoms of myasthenia gravis?

A

Muscle weakness e.g. partial and bilateral ptosis, diplopia, dysphagia

Fatiguability - symptoms are worse after repetitive movements and at end of the day

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63
Q

What is the main complication of myasthenia gravis?

A

Breathing difficulties (crisis/later on). Especially in water for example. Get type 1 rest failure

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64
Q

What are the bedside tests for MG?

A

Ice cube test - Put ice cubes/pack on eyelids and see if ptosis resolves

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65
Q

What are the blood tests for MG?

A

ntibodies - Anti-nAchR and Anti-MUSK (if anti-nAchR is -ve)

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66
Q

What imaging should be done for MG?

A

CT CAP - Thymoma is associated

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67
Q

What special tests should be done for MG?

A

Nerve Stimulation tests - decrease in amplitude following repeated stimulation

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68
Q

What is the medical management of MG for SYMPTOM RELIEF?

A

Acetylcholinesterase Inhibitors e.g. PO Pyridostigmine.

↑ availability of Acetylcholine.

Short half life so have to give several doses over the course of the day.

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69
Q

What is the medical management of MG for IMMUNE REGULATION?

A

Steroids e.g. IM methylprednisolone.

Preventative for relapse.

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70
Q

What is the medical management of MG for PREVENTION OF CRISIS OR BEFORE SURGERY?

A

IVIG. Destroys autoantibodies and prevents production of new autoantibodies

Plasmapheresis

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71
Q

What is the surgical management of MG?

A

Thymectomy - Thymic hyperplasia is a common association

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72
Q

What is an important Ddx for MG and how does it differ?

A

Lambert Eaton Myasthenic Syndrome (LEMS)

Paraneoplastic syndrome from small cell lung cancer

HOWEVER it is the pre-synaptic voltage gated calcium channels that are affected

SO you get the opposite whereby muscle weakness improves upon repetitive movements

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73
Q

What is the driving restriction following a seizure?

A

First unprovoked/isolated seizure: 6 months off if there are no relevant structural abnormalities on brain imaging and no definite epileptiform activity on EEG.

If either abnormality is present then the time increases to 12 months

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74
Q

What is the driving restriction following a syncopal episode? (4)

A

simple faint: no restriction

single episode, explained and treated: 4 weeks off

single episode, unexplained: 6 months off

two or more episodes: 12 months off

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75
Q

What is the driving restriction following a TIA or stroke?

A

4 weeks

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76
Q

What are the stages of raised intracranial pressure according to the Monro-Keillie Theory?

A

1 = compensated so CSF and venous loss to allow for expanding areas

2 = decompensated so no more volume loss and ICP rises but is still normal

3 = positive feedback = ICP greater than BP so oedema

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77
Q

What clinical signs are seen when the midbrain is compressed and why?

A

Reduced consciousness and GCS due to compression of the reticular formation

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78
Q

What clinical signs are seen when the pons is compressed and why?

A

Diplopia on horizontal gaze due to compression of CN VI

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79
Q

What clinical signs are seen when the medulla is compressed?

A

Nausea and vomiting

Usually happens late on

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80
Q

What clinical signs are seen when the brain and therefore optic nerve are compressed?

A

Papilloedema and reduced visual acuity

leakage of cellular components into optic disc = swelling

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81
Q

What clinical signs are seen when the brain and therefore arterioles are compressed?

A

Stimulation of Cushing’s response due to a reduction in cerebral perfusion pressure

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82
Q

What is Cushing’s Reflex?

A

Bradycardia

Hypertension

Respiratory Depression

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83
Q

Why does RICP cause a headache? What are the features?

A

Due to pressure on the pain receptors in vessels and meninges

Worse on straining/bending over and when waking in the morning

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84
Q

Why do the RICP headache features occur?

A

Coughing etc = raised intra-abdominal pressure reduces venous return form SVC so increases volume pressing on meninges

Sleep = physiological hypoventilation leads to vasodilation of cerebral vessels (CO2 retention)

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85
Q

What are the observations seen on fundoscopy of RICP?

A

Blurred disc margins and hyperaemia

Flame haemorrhages

Loss of venous pulsations

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86
Q

What are the causes of RICP? (5)

A

Focal oedema (Brain haemorrhage, trauma, infarction)

Neoplasms (mets, glioma, meningioma)

Infection (abscess, meningitis, encephalitis)

CSF disturbance

Idiopathic Intracranial Hypertension

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87
Q

What is the first stage of acute RICP treatment after confirming with a CT head?

A

Elevate head, admit to ITU and sedate

Anaglesia, IV fluids + inotropes

Other bits e.g ventriculostomy I don’t think you need to know them

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88
Q

What is the second stage of acute RICP after confirming with a CT head?

A

IV mannitol - osmotic diuretic so draws fluid back into the intravascular space

Hypertonic saline

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89
Q

What is the third stage of acute RICP treatment after confirming with a CT head?

A

Decompressive craniotomy

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90
Q

What are the layers of the scalp?

A

SCALP

S kin
C onnective tissue (dense)
A poneurosis
L oose connective tissue
P eriosteum
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91
Q

What is the clinical significance of the loose connective tissue in the scalp?

A

Emissary veins connect scalp to dural venous sinuses

no bony insertion for the aponeurosis = bleeding can occur peri-orbitally

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92
Q

What are the 3 layers of the meninges?

A

Dura mater

Arachnoid Mater

Pia Mater

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93
Q

Describe the Dura Mater. What is its significance

A

2 layers: periosteal and meningeal

Dural venous sinuses exist between layers along with lots of other vessels

94
Q

Describe the Arachnoid Mater. What is its significance

A

Loosely surrounds the brain

CSF exists in here which is for nutrition, protection and creation of a weightless environment

95
Q

How is CSF produced?

A

Produced by the choroid plexus in the lateral ventricles

Gravity allows drainage into 3rd ventricle, cerebral aqueduct and 4th ventricle

4th ventricle then allow drainage into SA space

96
Q

Describe the Pia Mater. What is its significance

A

Vacuum packs the brain for pathogen protection

v v thin

97
Q

Why do subarachnoid haemorrhages normally occur?

A

Spontaneous rupture of berry aneurysm

98
Q

How does encephalitis normally present?

A

A triad of fever, headache and a change in mental status

99
Q

What are the most common causes of encephalitis?

A

Viral - HSV, CMV or all childhood viruses

Bacterial - TB, listeria, legionella

Fungal and parasitic

100
Q

Which investigations should be done to diagnose encephalitis?

A

Bed - stool culture + throat swab

Bloods - All the bloods + blood film

Imaging - CT head to rule out RICP causes
MRI to detect demyelination

Special - LP + viral PCR

101
Q

Where does the spinal cord terminate?

A

Lower level of L1 so between L1 and L2

102
Q

What is the aetiology of cauda equine syndrome?

A

Compression or damage of the nerve roots below the level of the spinal cord

Iatrogenic following Spinal/epidural/LP

Trauma

Neoplasia

Lumbar stensosis

103
Q

How does cauda equina normally present symptom wise?

A

Pain - lower back +/- radiation down lower limbs

Saddle anaesthesia

Urinary retention + constipation/incontinence

LMN signs - hypotonia, weakness

Sexual dysfunction

104
Q

How does cauda equina normally present examination wise?

A

LMN signs + sensory impairment esp in perineum

Reduction in anal tone when both resting and contracting

palpable bladder

105
Q

Which investigations should be done to diagnose cauda equina?

A

All the bloods

MRI!

Or ct myelogram if not possible

106
Q

What is the management of cauda equina?

A

Urgent surgical decompression

107
Q

What is central cord syndrome? How does it normally present?

A

Extension injury to an osteoarthritic spine leads to cord injury in the central grey matter

Lower limb fibres are more lateral so are less affected

Compromised motor function and pain/temperature in upper limbs

108
Q

What is Horner’s syndrome?

A

Miosis

Partial ptosis (usually unilateral)

Anhidrosis on one side

Due to damage to the sympathetic trunk therefore reducing sympathetic innervation to eye and face

109
Q

Describe a cluster headache

A

Episodic eye pain (usually unilateral)

lacrimation

nasal stuffiness

occurring daily and lasts around 15 minutes

110
Q

What is the management of a cluster headache?

A

acute: 100% oxygen subcutaneous triptan

Prophylaxis: Verapamil

111
Q

How can the symptoms of a focal temporal epilepsy help to localise it?

A

HEAD

Hallucinations
Emotional/epigastric rising
Automatisms e.g. lip smacking/ pinching
Deja vu

112
Q

How can the symptoms of a focal parietal epilepsy help to localise it?

A

Sensory!

Parasthesia etc

113
Q

How can the symptoms of a focal frontal epilepsy help to localise it?

A

MOTOR

Head/leg movements

posturing

post-ictal weakness

Jacksonian march

114
Q

How can the symptoms of a focal occipital epilepsy help to localise it?

A

Visual

Floaters/flashes

115
Q

Give 3 drugs that may exacerbate a myasthenia crisis?

A

Bisoprolol/B blockers

Abx e.g. tetracycline/gentamicin

Lithium

116
Q

What are the 3 most common causes of foot drop?

A

Common peroneal nerve lesion

L5 radiculopathy

Sciatic nerve lesion

117
Q

How does a common peroneal nerve palsy normally present?

A

Weak dorsiflexion

Weak eversion

Normal reflexes

118
Q

How does a L5 radicuolpathy normally present?

A

Weak hip abduction

Weak dorsiflexion

Weak eversion and inversion

Parasthesia between the webbing of first and second toe

119
Q

What is the function of upper motor neurones? How would a lesion affect function?

A

A net inhibitory effect on LOWER motor neurones

Lesion = LOSS of inhibition of LMN = ↑ excitation

↑ number of action potentials = ↑ muscle contractions = ↑ tone

120
Q

What are the 4 main signs of an UMN lesion?

A

Hypertonia

Spasticity

Changes in reflexes

Clonus

121
Q

What is spasticity and how can it be elicited in an UMN lesion?

A

Continuous contraction of a muscle and paralysis of its antagonist

Pronator Drift - indicates spasticity as limbs trying to return to pathological position

UL = flexion dependent 
LL = extension dependent
122
Q

How do reflexes change following an UMN lesion?

A

Hyperreflexia

Babinski reflex

Clasp-knife reflex (quick ↓ in resistance following force)

123
Q

What is Babinski’s reflex?

A

Rubbing lateral side of the sole of the foot causing extension

Big toe dorsiflexes and the other toes fan out.

Normal in children up to 12 months old.

124
Q

What is clonus?

A

Series of involuntary and rhythmic muscular contractions and relaxations.

125
Q

What is the function of Lower Motor Neurones?

A

Link UMNs to skeletal muscle

Constantly firing so have to be inhibited by UMNs

126
Q

What are the 4 signs of a LMN lesion?

A

Hypotonia + reduced power

Hyporeflexia

Muscle wasting

Fasciculations

127
Q

What are fasciculations?

A

Uncoordinated contractions and relaxations of muscle due to ectopic Ach receptor expression

128
Q

How does an UMN lesion affect the facial muscles and why?

A

Paralysis of contralateral lower face. Cannot smile but can raise eyebrows

Upper half of face receives innervation from both contralateral and ipsilateral sides

129
Q

How does a LMN lesion affect the facial muscles and why?

A

Paralysis of ipsilateral upper and lower half of face. Cannot move one side

Lower half of face receives innervation from only the contralateral side

130
Q

How does a migraine normally present?

A

Headache - unilateral, throbbing +/- parasthesia

Prodrome - precedes by days/hours. mood/sleep changes

Aura - precedes headache by ~15-30mins. Visual changes/hemianopia

N&V

Light sensitivity
Mechanophobia
Motor features e.g. ataxia or hemiparesis

131
Q

What are the triggers of a migraine?

A 
CHOCOLATE covers ~50% cases
C hocolate
H angers
O rgasms
C heese/caffeine
O ral contraceptive pill
L ie ins
A lcohol
T ravel
E xercise

Realistically triggers are

  • changes to sleep pattern
  • stress
  • missing meals
  • dehydration
132
Q

What is the conservative management of a migraine?

A

Trigger avoidance - keep a headache diary

Pain management - warm/cool pack, rebreathing into a paper bag, acupuncture

133
Q

What is the acute medical management for a migraine?

A

NSAIDS/simple analgesia

Triptans at START OF HEADACHE

Anti-emetic e.g. metoclopramide/prochlorperazine

134
Q

What is the mechanism of action of triptans?

A

Serotonin 5-HT agonist = vasoconstriction

135
Q

What is the follow up management for a migraine?

A

Review in 2-8 weeks and see if preventative management is needed

136
Q

When would follow up management be needed for a patient with migraine?

A

Triptans and analgesia = treatment overuse headache

Affecting QOL

137
Q

What is the preventative management for migraine?

A

Monoclonal antibodies

propanolol

amitriptyline

Topiramate

138
Q

Should there be special consideration for females suffering with migraine?

A

YES

COCP is absolutely contraindicated if patient has migraine with aura

Give POP and advise to stop using immediately if they develop MWA.

139
Q

How do migraines change during pregnancy?

A

Often improves in pregnancy

If worsens then is associated with a greater risk of pre-eclampsia

140
Q

What is a bulbar palsy and which nerves are affected?

A

Disease affecting CNs due to LMN pathology so get LMN signs.

IX (glossopharyngeal)

X (Vagus)

XI (Accessory)

XII (Hypoglossal)

141
Q

What is the swallow reflex?

A

Soft Palate Stimulated and afferent nerve is CN IX (glossopharyngeal)

Goes to Trigeminal Nerve Nucleus then…

CN X = pharyngeal constriction
CN V = Jaw Opens
CN XII = Tongue thrusts

142
Q

How do the symptoms of bulbar palsy relate to the anatomy?

A

IX (glossopharyngeal) - Dysphagia = Unsafe swallow

X (Vagus) - Dysphagia and Dysphonia

XI (Accessory) - can’t shrug shoulders or turn head

XII (Hypoglossal) - Atrophic tongue, dysarthria, nasal voice

143
Q

What are 4 causes of bulbar palsy?

A

Acute = GBS (Rare)

Chronic = MND, MG, GBS, Syringobulbia

144
Q

Which investigations should be done for bulbar palsy?

A

CN Focussed Exam = Swallow? Speech? Shrug Shoulders? Turn Head? Eye movements? Look at tongue?

145
Q

What is a corticobulbar palsy?

A

UMN lesion affecting swallowing and speech muscles

Bilateral lesions (PD, Stroke, MS, MND) to corticobulbar tracts above the mid pons

UMN signs
Hyperreflexia of gag reflex
Slow and deliberate speech
Pseudobulbar affect - incongruent crying/laughing

146
Q

Define Brown Sequard syndrome

A

A complete hemisection of the spinal cord leading to both sensory and motor loss

147
Q

What are the CONTRALATERAL signs of Brown Sequard?

A

Contralateral loss of Spinothalamic Tracts (crude touch, pain, temperature) 2-3 levels below the level of the lesion

148
Q

What are the IPSILATERAL signs of Brown Sequard

A

Ipsilateral loss or Dorsal Columns (fine touch, proprioception and vibration) at the level of the lesion and below

Motor
Ipsilateral hemiplegia due to loss of Dorsal Horns (UMN signs) below the level of the lesion

Ipsilateral flaccid paralysis due to loss of Ventral Horns (LMN signs) at the level of the lesion

149
Q

What could cause a brown sequard syndrome?

A

Penetrating trauma e.g. stab wound

Vertebral fracture

V artery dissection

150
Q

What is the definition of cauda equina syndrome?

A

A collection of symptoms and signs that result from severe compression of the descending lumbar and sacral nerve roots.

151
Q

What are the symptoms and signs of cauda equina syndrome?

A

Symptoms
Saddle + anal anaesthesia
Pain (Lower back, Sciatic)

Signs
Loss of autonomic control e.g. bladder or bowel incontinence, sexual dysfunction

152
Q

Give 6 causes of cauda equina syndrome

A

Neoplasia - schwannoma, mets from prostate

Vascular - aortic dissection

Degenerative - spinal stenosis, lumbar disc herniation (L2-S2)

Inflammatory - Ank Stond

153
Q

Define spondylosis

A

A spinal condition resulting from degeneration and flattening of the intervertebral discs leading to pressure on the nerve roots

154
Q

What is the pathophysiology behind spondylosis?

A

Happens because of degeneration of the annulus fibrosis and osteophyte formation on the adjacent vertebra

= narrowing of canal and movement rubs the nerve over osteophytes

155
Q

How does spondylosis present?

A

Pain +/- Lhermitte’s Sign

Reduced movement and crepitus

Parasthesia

Muscle Weakness

Sensory loss
(depending on where the nerve root is)

156
Q

What is Lhermitte’s sign?

A

Electrical pain down the spine upon neck flexion

157
Q

What are the investigations to do for spondylosis?

A

XR = narrowing of disc space and osteophytes

URGENT MRI

158
Q

How should spondylosis be managed?

A

Conservative (Physio, Neck Brace/Lumbosacral corset)

Medical (Analgesia - NSAIDS/follow WHO ladder)

Surgical - Fusion of vertebrae

159
Q

What is Syringomyelia?

A

A cavity (syrinx) forms within the brainstem (bulbia) or spinal cord (myelia).

The syrinx is filled with CSF and expands outwards from the central canal AT THE SEGMENTAL LEVEL

160
Q

Which tracts are affected in Syringomyelia and why?

A

Spinothalamic Tracts - Bilateral loss = cape like distribution

Nerves cross AT THE SEGMENTAL LEVEL and so damaged area

161
Q

Which tracts are NOT affected in Syringomyelia and why?

A

Dorsal Columns

Nerves DO NOT CROSS AT SEGMENTAL LEVEL as ascend on ipsilateral side so not affected

Get DISSOCIAL sensory loss

162
Q

What are the myotomes for:

C4
C5
C6
C7
C8
A

C4 = shoulder shrugs

C5 = Elbow flexion

C6 = Wrist extension

C7 = Elbow extension and wrist flexion

C8 = Finger flexion and thumb extension

163
Q

What are the myotomes for

T1
L2
L3
L4
L5
A

T1 = Finger abduction

L2 = Hip flexion

L3 = Knee extension

L4 = Ankle dorsiflexion

L5 = Big to extension

164
Q

What are the myotomes for

S1

A

S1 = Ankle plantarflexion

165
Q

What is the definition of vitamin B12 deficiency

A

A common condition that can manifest with neurological, psychiatric and haem symptoms

166
Q

How does a B12 deficiency lead to anaemia?

A

B12 is a cofactor for enzymatic reactions in DNA synthesis (methionine synthesis) and FA metabolism

↓DNA synthesis = macrocytic anaemia + pancytopenia

Also ↓ conversion of homocysteine to methionine = neuropathy, glossitis and CVS disease

FA not metabolised = demyelination of nerves

167
Q

How does inadequate absorption of B12 occur?

A

↓ in Intrinsic Factor (Drugs - PPI or Metformin use, Atrophic gastritis (H. Pylori, Gastrectomy)

Terminal Ileum pathology (Ulcerative colitis/Crohns +/- a resection, Coeliac Disease, Pancreatic insufficiency)

168
Q

Give 2 other mechanisms for b12 deficiency?

A

Lack of dietary intake (found in meat and dairy) - Strict veganism, chronic alcohol use

Increased demand for B12 - Leukaemia, Pregnancy, Breastfeeding

169
Q

What is subacute degeneration of the spinal cord?

A

Loss of vibration and proprioception (Dorsal Columns) @ hands and feet

Progresses to sensory loss @ all modalities

Gait ataxia
Distal Muscle Weakness (esp legs)
+/- dementia features

170
Q

Which blood tests are for B12 deficiency?

A

FBC

Peripheral Blood
Smear

Serum B12

Reticulocyte Count

Autoantibodies - Anti-IF and Anti-Parietal Cell (pernicious anaemia)

171
Q

What is the management of B12 deficiency?

A

Replace via IM injections

Neuro symptoms might be irreversible 🤷🏽‍♀️

172
Q

What is the definition of diabetic neuropathy?

A

A highly prevalent complication of diabetes (type 1 or type 2) and is characterised by the presence of symptoms and/or signs of peripheral nerve dysfunction and/or autonomic nerve dysfunction.

173
Q

What is the pathophysiology behind Diabetic neuropathy?

A

Hyperglycaemia causes:
Ischaemia to nerves supplying small vessels

Inflammation to nerves

SO,
metabolic and vascular dysfunction leads to mitochondrial dysfunction
Leads to progressive and accumulative damage to nerves

174
Q

How would an EARLY diffuse diabetic neuropathy present?

A

Distal, symmetrical pattern of sensory loss

Glove and sto
cking distribution
Pain (prickling, burning, worse @ night)

Ulcers

175
Q

How would a late diffuse diabetic neuropathy present?

A

Autonomic dysfunction

Orthostatic Hypotension
Bladder/Bowel/Sexual dysfunction
GI - bloating, early satiety

176
Q

How would a diabetic mononeuropathy present?

A

Isolated nerve palsies e.g. CN, PN - foot drop, carpal tunnel

177
Q

What are the risk factors for diabetic neuropathy?

A

Non-Modifiable - Age, disease duration, Tall height

Modifiable - Lifestyle (smoking, obesity, poorly controlled hyperglycaemia), CVS (HTN, Hyperlipidaemia)

178
Q

What are 4 differentials for diabetic neuropathy?

A

B12 deficiency

Chronic Inflammatory Demyelinating Polyneuropathy (more motor)

GBS

Drug induced Neuropathy

179
Q

What are 3 complications of diabetic neuropathy?

A

Ulcers!!! (infection +/- gangrene, amputation, Charcot foot)

Depression

Silent MI

180
Q

What should you look for on examination when diabetic neuropathy is suspected?

A

Symmetrical, distal SENSORY loss
Reduced or absent ankle reflexes
? Ulcers
? Ataxia

181
Q

Which bedside tests should be done in diabetic neuropathy?

A

Baseline obs - BP for postural drop???

182
Q

Which blood tests should be done in diabetic neuropathy?

A

HbA1c, fasting blood glucose - is the diabetes well controlled?

B12 - exclude deficiency

FBC - exclude anaemia and other inflammatory disorders

TFTs, lipids?

183
Q

What is the conservative management of diabetic neuropathy?

A

Annual review

Supportive - help to manage glycaemic control

Self care education about feet (grim)

184
Q

What is the medical management of diabetic neuropathy?

A

Pain management

Pregablin/Gabapentin +/- duloxetine
Antidepressant
Opioid

Alpha 1 Agonist for autonomic dysfunction

185
Q

Define carpal tunnel syndrome

A

A clinical syndrome that occurs due to impingement of the median nerve (C7) as it passes underneath the flexor retinaculum

186
Q

What are the symptoms/signs of carpal tunnel?

A

Sensory changes in the C7 dermatome

Numbness
Parasthesia
Pain

Wasting of the thenar eminence

Clumsy

187
Q

What are the causes of carpal tunnel

Median Trap

A 
Myxoedema (hypothyroidism)
Edema

Diabetes Mellitus

Idiopathic

Acromegaly
Neoplasia

Trauma

Rheumatoid Arthritis, 
Amyloidosis

Pregnancy
188
Q

What are the risk factors for carpal tunnel?

A

Non-Modifiable

- Female
- Age (40-60)
- Hx wrist fracture
- Rheumatoid arthritis

Modifiable

- Lifestyle - smoking
- Occupation involving lots of wrist work
- Walking aids
189
Q

Give 2 investigations for carpal tunnel?

A

Tinel’s Test - Tap on median nerve at wrist + parasthesia = POSITIVE

Phalen’s Manoeuvre - Flex hands 30-60 degrees + parasthesia = POSITIVE

190
Q

What is the management of carpal tunnel?

A

Splint

NSAIDs

Cortiocsteroids

Surgical release

191
Q

What is the definition of MND?

A

A cluster of neurodegenerative diseases characterised by selective loss of neurones in the:

Motor Cortex
Frontotemporal
Cranial Nerve Nuclei
Bulbar (pons, medulla)
Anterior Horn Cells

usually due to cytotoxicity by glutamate excess

192
Q

Where is most affected by motor neurone disease?

A

Both UMN and LMN

BUT ABSOLUTELY NOT

sensory neurones (polyneuropathy and MS), sphincters and eye muscles (=movements like in myasthenia)

193
Q

What are the 3 types of MND?

A

Amyotrophic Lateral Sclerosis (UMN and LMN)

Primary Lateral Sclerosis (UMN)

Progressive Muscular Atrophy (LMN)

194
Q

What is the usual presentation of ALS? (5)

A

Proximal myopathy, foot drop, spastic gait = common

Progressive disability with no periods of remission or stability

Asymmetrical!!!

UMN and LMN signs

> 40 (usually)

195
Q

What is the management of MND?

A

Conservative (MDT involvement - Physio, OT, SALT, Education on end of life care and ways to improve QOL)

Medical (Riluzole - reduces Glutamate.
Anti-cholinergics (to stop dribbling ‘sialorrhoea’
Annual pneumococcal and flu vaccines)

Surgical
PEG can improve QOL

196
Q

What is the definition of muscular dystrophy?

A

A progressive, generalised diseases of muscle, most often caused by defective or specifically absent glycoproteins (e.g., dystrophin) in the muscle membrane.

Characterised by ongoing degeneration and re-generation of muscle fibres.

197
Q

What is the pattern of inheritance in both Duchenne and Beckers muscular dystrophy?

A

X-linked recessive

198
Q

What is the usual clinical presentation of muscular dystrophy?

A

Delayed motor milestones* e.g. head control by 4 months, walking by 18 months, running by 3 years

Waddling gait/tiptoe walking

Calf pseudohypertrophe (large due to fibrosis and fat)

Episodes of unexplained myoglobulinaemia

Gower’s Sign

199
Q

What is Gower’s sign?

A

Slowly try to get up from lying on tummy by using their arms

Due to symmetrical, proximal muscle weakness

200
Q

What are 3 later signs of muscular dystrophy?

A

Respiratory failure
Scoliosis
Dilated cardiomyopathy

201
Q

How do Duchenne and Becker’s MD differ?

A

D = Deficit of dystrophin. Symptoms are more severe and earlier onset (~5 years old). ID = common

B = Misshapen dystrophin. Symptoms are less severe and later onset (10-20)

202
Q

What is the conservative management of Muscular Dystrophy?

A

Physio and conditioning

Genetic counselling for parents

203
Q

What is the medical management of muscular dystrophy?

A

Glucocorticoids can prolong independent walking and improve muscle strength

However, also cause weight gain and behavioural abnormalities so have to weigh up choices

204
Q

What is the definition of Wernicke’s encephalopathy?

A

A neurological emergency resulting from thiamine deficiency with varied neurocognitive manifestations, typically involving mental status changes and gait and oculomotor dysfunction.

205
Q

How does chronic alcohol consumption lead to B1 deficiency?:

A

Conversion of Thiamine to its active form

Absorption of Thiamine @ the Duodenum

Storage of Thiamine in the liver due to cirrhosis
(and also causes malnutrition)

206
Q

What is the triad of symptoms seen in Wernicke’s?

A

Ataxia

Autonomic Instabiity

Nystagmus

(+ confusion)

207
Q

What is the management for Wernicke’s?

A

Pabrinex/IV B1 - Levels need to be corrected before giving glucose otherwise there won’t be a glycolysis mechanism = lactic acidosis

208
Q

What is the definition of Korsakoff’s syndrome?

A

A residual syndrome in patients who suffered from a Wernicke encephalopathy and did not receive appropriate treatment at that time. It is chronic and irreversible.

209
Q

What are the symptoms of Korsakoff’s?

A

Retrograde and anterograde amnesia

Confabulation

210
Q

What is the definition of Horner’s syndrome?

A

Compression of the sympathetic chain leads to reduced sympathetic innervation to head and neck.

211
Q

What is the triad of symptoms seen with Horner’s?

A

Partial ptosis (Reduced innervation to Superior Tarsal Muscle so can’t elevate eyelid)

Unilateral anhidrosis

Miosis (Reduced innervation to Dilator Pupillae so can’t dilate)

212
Q

Give 4 causes of Horner’s syndrome

A

Vascular - ICA dissection, Cavernous sinus thrombosis, lateral medullary syndrome

Inflammatory - Syringomylia


Trauma - Atlas fracture

Neoplasia - Pancoast Tumour

213
Q

Give 3 ddx for ptosis and how they differentiate from each other

A

CN III lesion - Ptosis is unilateral and complete

Sympathetic Lesions e.g. Horners - Ptosis is unilateral and partial

Myopathy - Ptosis is bilateral and partial e.g. MG

214
Q

Define temporal arteritis

A

Granulomatous vasculitis of large and medium-sized arteries. It primarily affects branches of the external carotid artery, and it is the most common form of systemic vasculitis in adults.

215
Q

What are the branches of the external carotid artery

A

Some Angry Ladies Figured Out PMS

Superior Thyroid
Ascending Pharyngeal
Lingual
Facial
Occipital
Posterior Auricular
Maxillary
Superficial Temporal
216
Q

How does temporal arteritis normally present?

A

Headache over the temporal region (HEADACHES IN >50 ARE GCA UNTIL PROVEN OTHERWISE AS CAN HAVE PERMANENT VISUAL LOSS)

Optic neuropathy/visual disturbances?
Monocular sudden loss of vision/Amaurosis Fugax

Weight Loss
Fatigue, malaise
Sweats
Jaw claudication

Vessels can become tender, thick, nodular and pulsatile = Occlusion

217
Q

What are the non-modifiable risk factors for temporal arteritis?

A

Age >50
Female > Male
Caucasian > other ethnicities
Hx of Polymyalgia Rheumatica

218
Q

What are the modifiable risk factors for temporal arteritis?

A

Smoking
Other CVS risk factors e.g. atherosclerosis
Investigations

219
Q

Which blood tests should be done in temporal arteritis?

A

ESR - Raised in GCA. If ESR is not raised then it isn’t GCA.
LFTs - Raised ALP
IgG - Raised
Creatine Kinase is not raised (no muscle damage)

220
Q

What diagnostic investigation should be done in temporal arteritis?

A

Temporal Artery biopsy is gold standard
Have to do serial sectioning and large segments incase a bit is missed
Shows mononuclear cells that have joined together to form giant cells

221
Q

What is the management of temporal arteritis?

A

PO prednisolone

222
Q

What are the typical features of a post-lumbar puncture headache?

A

develops within 24-48 hours following LP but may occur up to one week later

may last several days

worsens with upright position

improves with recumbent position

223
Q

What is the management of a post-lumbar puncture headache?

A

Supportive - analgesia, fluid, rest

IV caffeine, blood patch, epidural saline if more than 72 hours

224
Q

Define Bell’s palsy

A

An acute, unilateral, idiopathic, facial nerve paralysis.

225
Q

What are the features of Bell’s palsy?

A

lower motor neuron facial nerve palsy - forehead affected i.e. forehead not spared

patients may also notice post-auricular pain (may precede paralysis), altered taste, dry eyes, hyperacusis

226
Q

What is the triad seen in normal pressure hydrocephalus?

A

urinary incontinence
dementia and bradyphrenia
gait abnormality (may be similar to Parkinson’s disease)

227
Q

Define degenerative cervical myelopathy

A

Spinal cord dysfunction that occurs when age-related osteoarthritic changes cause narrowing of the cervical spinal canal, leading to chronic spinal cord compression and neurologic disability.

228
Q

How does degenerative myelopathy present?

A

Pain
Loss of motor function

Loss of sensory function causing numbness

Loss of autonomic function (urinary or faecal incontinence and/or impotence

Hoffman’s sign:

229
Q

What is Hoffman’s sign?

A

A reflex test

gently flick one finger on patient’s hand.

A positive test = in reflex twitching of the other fingers on the same hand in response to the flick.

230
Q

What is the gold standard test for degenerative myelopathy?

A

An MRI of the [cervical] spine

It may reveal disc degeneration and ligament hypertrophy, with accompanying cord signal change.

231
Q

What is the treatment for degenerative myelopathy?

A

Decompressive surgery

232
Q

Should the DVLA be informed after a provoked seizure?

A

Yes

The patient has to inform them and it is their decision whether they can drive again

(probably ok if they’re provoked)

EOY4 (22 decks)

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