Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MD2 Neuro > Worsening Weakness and Numbness > Flashcards

Worsening Weakness and Numbness Flashcards

1
Q

Helen, 29, presents with painless numbness in lower limbs

PHx: non significant

Smoker, occasional alcohol, no illicit drugs

FHx: mother has Graves disease

Social: full time pharmacy assistant, just married

What other questions would you like to ask?

A

Location of numbness (including sensory level)

Course

Onset

Duration

Other symptoms (e.g. visual disturbance, bowel and bladder symptoms including frequency, urgency and incontinence)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Helen, 29, presents with painless numbness in LLs

Started under L foot, moved up L leg and progressed to ribcage

Gradual increase in intensity and extent over 2 weeks

Other Sx: less severe numbness in R leg/foot, mild bilateral leg weakness, “can’t walk properly, worse in evenings, after my shower/bath”

Other questions on systems review? Why are you asking each of these?

A

Back pain, trauma

Sx not worse wih cough/sneeze or valsalva: suggests compressive aetiology (e.g. root lesion, any pathology causing an underlying acute back pain) which is exacerbated by increased intrathoracic pressure

Systemic AI disease

Rashes or arthralgia: SLE (usually a brain problem, doesn’t affect rest of CNS)

Miscarriages: anti-phospholipid syndrome

Dry mouth, dry eyes: Sjogren’s syndrome

Recent infections: para-infectious causes, GBS

Recent vaccinations: GBS

Diet restriction (esp veganism): B12 deficiency

B symptoms/paraneoplastic syndromes: malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How can Sjogren’s syndrome affect the CNS?

A

Can produce inflammatory change in spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What paraneoplastic syndromes can affect the CNS?

A

Paraneoplastic cerebellar degeneration (typically in small cell lung cancer), causing ataxia

Peripheral neuropathy (chronic sensorimotor neuropathy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Helen, 29, presents with painless numbness in LLs

Started under L foot, moved up L leg and progressed to ribcage

Gradual increase in intensity and extent over 2 weeks

Other Sx: less severe numbness in R leg/foot, mild bilateral leg weakness, “can’t walk properly, worse in evenings, after my shower/bath”

Where in the nervous system could the problem be?

A

Hx very compatible with inflammatory cord disorder due to the age of the patient and the fact there is no associated pain around the likely affected region

Problem is in spinal cord; brain or peripheral nerve disorder would not affect one side of trunk up to a specific level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Helen, 29, presents with painless numbness in LLs

Started under L foot, moved up L leg and progressed to ribcage

Gradual increase in intensity and extent over 2 weeks

Other Sx: less severe numbness in R leg/foot, mild bilateral leg weakness, “can’t walk properly, worse in evenings, after my shower/bath”

Summarise these Sx

A

Paraparesis with sensory level

Heat sensitive symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Uhthoff’s phenomenon

A

Reversible and stereotypic decrements in physical and cognitive Sx due to increased ambient body temperature (including exercise, fever, summer, hot showers)

Relatively specific for MS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Lhermitte’s sign

A

Electrical sensation that runs down the back and into the limbs, elicited by bending the head forward

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe a simplified approach to determining the anatomical cause of sensory loss

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe a simplified approach for localisation of the cause of neurological symptoms

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are 3 clinical features suggestive of a spinal cord pathology over a peripheral neuropathy?

A

Sensory level

Hyperreflexia

Bowel and bladder problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are 2 clinical features suggestive of a peripheral neuropathy over a spinal cord pathology?

A

Glove and stocking, dermatomal or single nerve distribution

Loss of reflexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

DDx for subacute paraparesis

A

Spinal cord pathology: MS, tumour

Peripheral nerve lesions: GBS (acute demyelinating polyradiculopathy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What features of Helen’s case are not consistent with GBS as an underlying cause?

A

Classically no sensory loss (and would not have a sensory level)

Weakness pattern usually distal in UL and proximal in LL

Weakness is the primary feature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

DDx for acute paraparesis

A

Trauma

Spinal cord stroke or SAH (usually in people with advanced arteriopathy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the cardinal feature of spinal cord stroke?

A

Rapid weakness but preservation of dorsal column function, because stroke almost always involves the anterior spinal supply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Helen, 29, presents with painless numbness in LLs

O/E: normal cranial nerve examination, normal UL examination, LL examination revealed few beats of clonus at L ankle, mild pyramidal pattern of weakness in both legs (worse on the L), brisk reflexes, upgoing plantar responses, loss of light touch and vibration up to T4, anal sphincter tone normal

Localise the lesion

A

UMN signs with a sensory level confirming this is in the spinal cord above or at T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Helen, 29, presents with painless numbness in LLs

UMN signs with a sensory level confirming this is in the spinal cord above or at T4

Ix?

A

MRI cervical and thoracic spine (lumbosacral goes from conus medullaris downwards as the spinal cord has already finished at this level; the conus is included in the thoracic anyway)

Somatosensory evoked potentials (SEPs)

Lumbar puncture: look for evidence of an inflammatory process (in MS: presence of oligoclonal bands in CSF and absence in blood serum, in neuromyelitis optica: anti-aquaporin Abs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Neuromyelitis optica

A

Neuromyelitis optica (NMO), also known as Devic’s disease or Devic’s syndrome, is a heterogeneous condition consisting of the simultaneous inflammation and demyelination of the optic nerve (optic neuritis) and the spinal cord (myelitis)

Can be monophasic or recurrent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What does Helen’s MRI show?

A

Ovoid inflammatory lesion in the cervical cord (“plaque”)

Confirms the Dx of a partial transverse myelitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is inflammatory myelitis?

A

Inflammatory demyelination of segment(s) of spinal cord

Functionally transects the cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Causes of transverse myelitis

A

MS (common)

Infectious/parainfectious inflammation (HSV, EBV, VZV, syphilis, Lyme)

Other AI disorders (vasculitis, systemic AI diseases)

No specific aetiology (40%; prognosis usually good so long as brain looks okay on imaging and there is no Hx of demyelinating lesions in the brain that would suggest MS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Possible complication of VZV infection in immunosuppressed patients

A

Necrotising myelitis (in association with shingles)

24
Q

Helen has an MRI brain performed

CSF: protein 0.38 g/L (N 0.15-0.40), cells 4/uL (3 lymphocytes and 1 erythrocyte; N), glucose 3 mmol/L (N), OCBs positive (without corresponding IgG in the serum)

Visual evoked potentials: normal

What are OCBs? Are these results in keeping with a transverse myelitis?

Dx?

A

Oligoclonal bands represent immunoglobulin produced by clonally expanded plasma cells; if not present in the blood serum, this indicates that a subpopulation of Abs have been created inside the intrathecal space and this is a specific finding for CNS inflammation/infection

Consistent with a transverse myelitis (cells may be mildly elevated)

Dx: clinically isolated syndrome (CIS) of MS (first clinical presentation compatible with the Dx of MS but not fulfilling the MS diagnostic criteria)

25
Q

What are the 4 most common first presentations of MS?

A

Transverse myelitis

Optic neuritis

Brainstem/cerebellar presentations (ataxia, nystagmus, vertigo, diplopia)

Incidental or with fatigue/non-specific Sx (nowadays more common)

26
Q

How is MS diagnosed?

A

Dissemination in space in the CNS: presence of documented neurological symptoms/signs in at least 2 functional systems of the CNS (e.g. transverse myelitis AND optic neuritis), as supported by radiological findings (lesions in at least 2 regions of the CNS)

Dissemination in time: at least 2 relapses at least 1 month apart, with at least 2 lesions of different age on imaging

27
Q

DDx for MS

A

Neuromyelitis optica (NMO, Devic’s disease)

Other systemic AI diseases

Acute disseminated encephalomyelitis (ADEM)

Sarcoidosis

Infections (e.g. brain abscess)

Tumours

Conversion disorder, somatisation

28
Q

Acute disseminated encephalomyelitis

A

ADEM is a rare AI disease marked by a sudden, widespread attack of inflammation in the brain and spinal cord

Can be post-viral, post-vax

29
Q

Causative organisms for brain abscess

A

GAS

Nocardia

30
Q

What is the most common presentation of systemic sarcoidosis?

A

Pulmonary involvement (SOB, cough, fatigue)

31
Q

Characteristic appearance of sarcoidosis on XR

A

Bilateral hilar lymphadenopathy (bilateral enlargement of LNs of pulmonary hila); describes the enlargement of mediastinal LNs and is most commonly identified by a CXR

32
Q

What is a cold abscess?

A

A patient with a cold abscess does not appear systemically unwell

33
Q

What factors are predictive for a second attack of MS?

A

High predicted by number of inflammatory lesions on baseline MRI brain (Helen had 1 spinal and several brain lesions)

Presence of OCBs in CSF confers additional risk

34
Q

What is MS? Describes its epidemiology, pathogenesis, presentation and natural Hx

A

AI demyelinating disease of the CNS

Most common neurological disease affecting young people in Aus

Characterised by inflammation, demyelination and axonal degeneration

Neurological Sx can be inflammatory (acute) and degenerative (chronic)

Course usually relapsing and remitting, usually followed by secondary progression

35
Q

Describe the 3 main subtypes of MS

A

Relapsing-remitting MS (RRMS; most common): relapses with complete or incomplete recovery and stable phase between relapses

Secondary progressive MS (SPMS): 50-75% of RRMS cases become SPMS within 15 years, gradual neurological deterioration, with or without superimposed relapses

Primary progressive MS (PPMS; 10%): gradual but continuous neurological deterioration, if relapses occur it is called progressive-relapsing MS

36
Q

What factors are suggestive of a better prognosis in MS?

A

Female, young (onset before 35)

Initial sensory Sx and optic neuritis (as opposed to motor or cerebellar dysfunction)

Initial mono-symptomatic presentation

Sudden onset, good recovery, lower attack rates, longer attack intervals

37
Q

Describe the natural Hx of MS

A

1/3 do well without accumulating significant disability

1/3 accumulate neurological deficits to impair activities but not serious enough to prevent them from leading a normal life

1/3 become disabled and require gait/mobility aids and even high level care

38
Q

Helen’s numbness improves without treatment over 3/52

10/12 later: pain behind the L eye worse with eye movement, visual acuity reduces from 6/5 baseline to 6/9 (two lines on acuity chart), colour desaturation in L, papilloedema in L on fundoscopy

How can colour desaturation be assessed?

Dx?

A

Ishihara plates, or ask patient to cover bad eye, show them something red, then ask them to swap eyes and see if there is any reported difference

Dx: acute optic neuritis (this second attack or relapse confirms her Dx of clinically definite MS)

39
Q

How is MS relapse defined? What is the prognosis of a relapse?

A

Episode of neurological disturbance consistent with MS which lasts for at least 48 hours (but usually 2-4 weeks; note the 48-hr cut-off is a research definition and patients may report shorter episodes) and occurs at least 30 hours from onset of last attack; is not preceded by a viral-like illness

Usually there is good recovery but residual disability may persist

40
Q

Mx of MS relapse

Why can’t an oral at-home option be used?

A

3-5/7 of IV methylprednisolone 1g/day to reduce severity of attack and shorten recovery time (although effect on ultimate recovery is uncertain

Also give prophylactic slow K

Oral prednisolone has not be shown to work in this clinical context, although it has recently been demonstrated that large doses of oral methylprednisolone may be effective (but not generally used)

41
Q

SEs of IV methylprednisolone

A

Agitation (sleep disturbance, psychosis, mania)

Hypokalaemia (give prophylactic slow K!)

HTN

Hyperglycaemia

Peptic ulcer disease (esp if also on NSAIDs)

Body fat redistribution (“moon face”)

OP

AVN

Cataracts

Skin changes

Increased infection risk (immunosuppression)

42
Q

Following the course of steroids, Helen’s acute optic neuritis subsides; her retrobulbar pain resolves, her visual acuity recovers to 6/7.5, her colour vision recovers to normal and fundoscopy shows a pale optic disc in her L eye

Significance of pale optic disc?

Long term MS Mx?

A

Pale optic disc indicates optic atrophy

Long term MS Mx: no cure so disease modifying therapy is the mainstay of treatment

Goals of treatment are prevention of relapses and/or new MRI lesions, and prevention of disability progression

43
Q

List disease modifying therapies currently available for the treatment of MS

A

1st tier: interferons B (SC or IM injections 1-4/week), glatiramer acetate (daily SC injections), teriflunomide (daily tablet)

2nd tier: fingolimod (daily tablet), dimethyl fumarate (BD tablet)

3rd tier: natalizumab (monthly infusion), alemtuzumab (2 infusion courses over 5 years)

44
Q

Common presentations of MS relapses (in descending order of incidence)

A

Sensory

Pyramidal

Visual

Brainstem

Cerebellar

Sphincteric

Cognitive

NB A Hx of certain relapse presentation predisposes patients to experiencing simiar relapses in the future (i.e. relapses tend to recur)

45
Q

What is pyramidal weakness?

A

Predominantly flexion weakness in LL (hip flexion, knee flexion, ankle dorsiflexion) or extension weakness in UL

46
Q

Common permanent MS symptoms

A

Fatigue

Walking difficulties

Bowel and bladder symptoms (frequency, urgency, incontinence)

Pain and other sensations

Visual disturbances

Cognitive problems

Tremors

Sexual dysfunction

Inability to work

Depression (reported by 14% of patients; suicide is 7-14x more common than general population)

47
Q

One year later, Helen’s disease has remained stable with no relapses, no new symptoms/signs and no new lesions on her brain and spine MRI

However she has been depressed for the past 3/12, with loss of interest in her usual hobbies, poor social life and insomnia

Mx of Helen’s depression?

A

Start symptomatic therapy with SSRI (e.g. escitalopram 10mg daily) OR commence psychotherapy (insufficient evidence to support combination therapy of depression)

48
Q

Possible social consequence to consider in a young person with chronic illness

A

Relationship changes

Financial

Demands at work, diminished employment opportunities

Study

Wanting children, fertility (consider medication SEs), sexual dysfunction

Young family

Adjustment, grief, fear of unknown

Low self esteem

Independence vs care needs

49
Q

In Helen’s 30s, she has 2 minor relapses over next 10 years, including an episode of diplopia and mild imbalance lasting 2/52, and L LL numbness and weakness again for 1/12

Receives 2/52 inpatient rehab program and DMT is changed to fingolimod

What parties are required for effective multidisciplinary Mx of MS?

A

Neurology

Rehab physicians

Continence/urology

Pain

Psychology

Patient support groups (MS society)

50
Q

What kinds of supports does formal rehab provide?

A

Symptomatic and supportive therapies: multidisciplinary involvement (medical, nursing, PT, OT, ST, psychology, SW)

May be inpatient or outpatient/community-based

Problem-solving education process

51
Q

What are the goals of rehab in MS?

A

Improve/maintain functional independence (transfers, mobility, personal care)

Modify environment and adaptive equipment

Addressing psychosocial and environmental factors

Caregiver education and support (reduce burden of care)

52
Q

How can fatigue be managed in MS?

A

Education: avoid heat, consider air conditioning, adequate sleep, good hygiene, good diet, adequate exercise

OT: teach pacing and work simplification strategies, provide equipment to minimise effort and energy consumption, involve employer to work on flexible work hours or work at home options, transportation (OT driving assessment), accessible work environment (e.g. location of bathrooms), memory aids, air conditioning

PT: aids for walking to improve gait efficiecny, home exercise program to improve fitness and aerobic capacity/endurance, improve well-being

Medication options include amantadine and modafinil

53
Q

Helen retires early (40-50s) due to deterioration in gait and repeated falls (experiences weakness, spasticity, ataxia/incoordination, imbalance, fatigue)

Dx? Mx?

A

Secondary progressive MS

Cease fingolimod (no evidence of effect of disease-modifying therapy in progressive MS)

Degeneration may be reduced by treatment in the RR phase with e.g. B-IFN, alemtuzumab, natalizumab, but not for secondary progressive

54
Q

Risk with use of monoclonal Abs e.g. natalizumab, alemtuzumab

A

Increased risk of JC virus which causes PML (progressive multifocal leukoencephalopathy)

55
Q
A

MD2 Neuro (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions