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Year 3 - MedEd Lectures > Neuro 2 > Flashcards

Neuro 2 Flashcards

1
Q

Define Multiple Sclerosis

A

A chronic, inflammatory, multifocal, demyelinating disease of the CNS. It results in:

Loss of myelin

Oligodendroglial and axonal pathology

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2
Q

What are the most common presenting symptoms of MS?

A

Optic Neuritis

Motor Weakness

Sensory Disturbances

Fatigue

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3
Q

What are the main risk factors for Multiple Sclerosis?

A

Nordic origin - living at higher latitudes

Autoimmune Conditions

HLA DLRB1*15

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4
Q

What are the main types of MS?

A

Relapsing-Remitting (Most common)

Secondary Progressive (Usually develops from RR)

Primary Progressive

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5
Q

How do you disagnose a patient with MS?

A

Absence of alternative diagnosis

Lesions are disseminated in Time and Space

Brain MRI - Plaques in white matter

CSF Studies

VEPs

Oligoclonal Bands in the CSF NOT the serum (shows location of inflammation to be solely within the CNS)

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6
Q

What are the key presenting symptoms of Myasthenia Gravis?

A

Muscles fatigue with use

Ptosis

Diplopia

Dysarthria

Dysphagia

SOB

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7
Q

Describe the pathophysiology of Myasthenia Gravis.

A

Antibodies target ACh receptors at the NMJ. Leads to fatigueability as more ACh is required with prolonged use of muscles.

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8
Q

How would you investigate a suspected case of Myasthenia Gravis?

A

Associations with Thymus Disorders.

Anti-AChR or Anti-MuSK antibodies

EMG

CT/MRI

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9
Q

What is Lambert Eaton Myasthenic Syndrome?

A

Weakness where muscles improve with use

Difficulty walking

Weakness in upper arms and shoulders

Dry Mouth, Constipation, Incontinence

Hyporeflexia

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10
Q

How would you diagnose a suspected case of Lambert-Eaton?

A

Associated with Small-Cell Lung Cancer & Autoimmune Diseases

Bloods - Anti-VGVC Antibodies

EMG

CT/MRI

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11
Q

What is Motor Neurone Disease?

A

Chronic Neurodegenerative disease causing muscle wasting, paralysis and death from respiratory failure.

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12
Q

How does MND present?

A

Progressive muscle weakness (spastic)

Dysphagia

SOB

Sparing of oculomotor, sensory and autonomic function

Bulbar Signs (Imparied swallowing and speech)

BOTH UMN and LMN symptoms

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13
Q

How would you investigate a suspected case of MND?

A

Clinical Diagnosis - investigate to exclude other possible diagnoses.

EMG

CT/MRI

Bloods (Serology, B12, CK)

Muscle Biopsy may be considered

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14
Q

How does Parkinson’s present?

A

Bradykinesia

Rigidity

Resting Tremor

Monotonous, hypotonic speech

Micrographia

Hypomimesis

March a petit pas (Shuffling Gait)

Misery

Memory Loss

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15
Q

What causes Parkinson’s Disease?

A

Degredation of dopaminergic neurones in the Substantia Nigra.

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16
Q

How does Parkinson’s Disease progress?

A

80% of neurones must be destroyed for a patient to become symptomatic.

1) Nigrostriatal Pathway - Motor symptoms
2) Mesolimbic/Mesocortical Pathways - Cognitive Symptoms

17
Q

Describe the epidemiology of Parkinson’s and its Risk Factors.

A

Typical patient would be an old man living in the countryside.

FHx increases risk 3x

18
Q
A
19
Q

What is Parkinson’s Disease dementia?

A

Similar to Lewy Body Dementia. Develops many years after Parkinson’s motor symptoms present.

Presents with:

Amnestic, language difficulties

Visuospatial Dysfunction (Neglect)

Hallucinations (Less Common)

Aggression

20
Q

What are the main types of Dementia?

A

Alzheimer’s (Most common)

Lewy Body Dementia (and Parkinson’s)

Vascular Dementia

Frontotemporal Dementia

21
Q

What are the key symptoms associated with Dementia?

A

Cognition and memory impairment.

Changes in motivation and attention

Changes in personality and behaviour

22
Q

What are the key symptoms of Alzheimer’s Dementia?

A

Amnesia - Remembering

Anomia - Naming

Apraxia - Doing

Agnosia - Recognising

Aphasia - Speaking

23
Q

In which area of the brain would you expect to see degeneration in a patient experiencing deficits in episodic memory?

A

Hippocampus

24
Q

Describe the pathophysiology of Alzheimer’s.

A

Amyloid plaques form from abnormally degraded amyloid precursor proteins. they form plaques, leading to degradation and inflammation.

Inside - Tau proteins tangle, causing atrophy and decreased ACh

25
Q

What are the main Risk Factors for developing Alzheimer’s?

A

Age

female

Vascular (DM, HTN, Dyslipidaemia, Diet)

Trauma

26
Q

What is Chronic Traumatic Encepalopathy?

A

‘Punch Drunk Syndrome’

Acute head injury seems to increase inflammation and amyloid levels within the brain. Associated with late-life risk of Alzheimer’s.

27
Q

How can you investigate a possible case of Alzheimer’s Disease?

A

CSF - High Tau Proteins, Low Amyloid.

CT/MRI show atrophy in late stages.

Tissue required for definitive diagnosis.

PET/SPECT are possible future diagnostic tools.

MMSE, MOCA

28
Q

What is Vascular Dementia?

A

Neuronal death occurs due to infarction; multiple strokes damage the small and medium sized vessels of the brain.

As such, risk factors closely match those of CVS disease.

Often displays stepwise progression.

29
Q

What is Pick’s Disease?

A

Form of dementia only affecting the frontal and temporal lobes.

Only caused by tau proteins, not amyloid plaques.

30
Q

How does Pick’s Disease present?

A

Personality Changes

Disinhibition

Overeating (sweet foods)

Emotional Blunting

Relative preservation of memory v other dementias

Presents earlier (40-60)

31
Q

What is Wernicke’s Encepalopathy?

A

Thiamine (B1) Deficiency leading to acute neurological signs.

Triad = Ataxia, confusion, eye signs

Typically occurs in malnourished alcoholics.

32
Q

What are the eye signs seen in Wernicke’s Encepalopathy?

A

Opthalmoplegia

Nystagmus

Diplopia

Ptosis

33
Q

What are the main causes of Wernicke’s Encepalopathy?

A

Alcoholism

Malnutrition

Bariatric Surgery

Dialysis

34
Q

How would you investigate a patient with suspected Wernicke’s Encepalopathy?

A

Serum Albumin and Vit B1

ECG

CT
Neuropsychology

35
Q

How would you manage a patient with confirmed Wernicke’s Encepalopathy?

A

Immediately give Pabrinex (B1)

36
Q

What is Huntington’s Disease?

A

Autosomal Dominant neurodegenerative disorder causing both motor and cognitive symptoms.

37
Q

How does Huntington’s present?

A

Motor

Chorea - Rapid jerky movements

Athetosis - Writhing hand movements

Ataxia

Dysphagia

Cognitive

Lack of concentration

Depression

Dementia

Personality changes

38
Q

What causes the symptoms of Huntington’s?

A

Atrophy of the caudate and putamen.

Global atrophy seen in advanced disease.

39
Q

How would you investigate a suspected case of Huntington’s Disease?

A

CAG codon repeat testing.

The more CAG repeats, the more likely the patient to develop the disease.

MRI/CT - Caudate/Striatal Atrophy in advanced disease.

Year 3 - MedEd Lectures (29 decks)

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