Station Neuro Flashcards

1
Q

What are Red flag symptoms of neck pain?

A

A serious underlying cause is more likely in people presenting with:
New symptoms before the age of 20 years or after the age of 55 years.
Weakness involving more than one myotome or loss of sensation involving more than one dermatome.
Intractable or increasing pain.
Red flags suggesting possible malignancy, infection or inflammation:
Fever.
Unexplained loss of weight.
History of inflammatory arthritis.
History of malignancy, drug misuse, tuberculosis, AIDS, or other infection.
Immunosuppression.
Pain that is increasing, unremitting and/or disturbs sleep.
Lymphadenopathy.
Exquisite localised tenderness over a vertebral body.
Red flags suggesting myelopathy (compression of the spinal cord):
Insidious progression.
Gait disturbance; clumsy or weak hands; loss of sexual/bladder/bowel function.
Lhermitte’s sign (flexing the neck causes electric shock-like sensations that extend down the spine and shoot into the limbs).
Upper motor neurone signs in the lower limbs (Babinski’s sign - up-going plantar reflex, hyperreflexia, clonus, spasticity).
Lower motor neurone signs in the upper limbs (atrophy, hyporeflexia).
Variable sensory changes (loss of vibration and joint position sense more evident in the hands than in the feet).
Red flags suggesting severe trauma/skeletal injury:
History of trauma.
Previous neck surgery.
Osteoporosis or risk factors for osteoporosis.
Increasing and/or unremitting pain.
Red flags suggesting vascular insufficiency:
Dizziness and blackouts (restriction of vertebral artery) on movement, especially on extension of the neck with upward gaze.
Dizziness, drop attacks.

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2
Q

What are your differentials?

A

Main Diagnosis = Nerve Root compression or radiculopathy (C5 nerve root),Brachial plexus injury,Focal neuropathy along the course of nerve(injury)
Other differentials = Stroke (lacunar), MS,mypoathy

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3
Q

What are the causes of nerve root compression?

A

cAUSES-trauma,herniated disc,cervical spondylosis,infection malgnancy,bracheal plexus pathology

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4
Q

What investigations would you do?

A

Bedside-observation,Peak floe,blood glucose(depending on presentation)

Blood-FBC(infection),U&E’s(CK-myopthies)LFT(malnourished).Bone profile(bone malignancies,ESR & CRP,B 12 and folate

Imaging- X-ray-trauma,MRI,emg,Nerve conduction studies

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5
Q

What is your management?

A

Management

  • Ifred flags(suggesting a serious spinal abnormality) are present,refer urgently or arrange immediate assessment, depending on clinical judgement. If the person has severe or progressive motor weakness, or severe or progressive sensory loss, seek immediate specialist advice.
  • Ifcervical radiculopathyhas been present for less than 4–6weeks and there are no objective neurological signs, provide conservative management:
    • Provide reassurance and information — the long-term prognosis of people with radiculopathy is good and most cases improve without surgery.
    • Encourage activity (includinghome exercise) and a return to a normal lifestyle (including work) as soon as possible.
      • However, advise the person not to drive if the range of motion of the neck is restricted.
      • Discourage the use of cervical collars because this restricts mobility and may prolong symptoms.
    • Advise that a firm pillow may provide comfort at night. It should provide lateral support and support the hollow of the neck and the position should be comfortable. Using two pillows may force the head into an unnatural position.
    • Offer oral analgesics(for example, ibuprofen, paracetamol or codeine)— thechoice depends on the severity of pain, personal preferences, tolerability, and risk of adverse effects.
    • Consider offeringamitriptyline, duloxetine, pregabalin or gabapentin. For more information, see the CKStopic onNeuropathic pain - drug treatment.
    • Consider prescribing muscle relaxants. For information on prescribing diazepam, see the CKS topic onBack pain - low (without radiculopathy).
    • Consider a referral forphysiotherapy —this may include strengthening andstretching exercises, andmanual therapy.
  • If cervical radiculopathyhas been present for 4–6 weeks or more,orthere are objective neurological signs:
    • Refer to confirm the diagnosis with magnetic resonance imaging (MRI), and to consider invasive procedures, such as interlaminar cervical epidural injections, transforaminal injections, or spinal surgery.
    • Indications for surgery include signs and symptoms of cervical radiculopathy, andcervical radiculopathy with unremitting radicular pain despite 6 to 12 weeks of conservative treatments, or progressive motor weakness, and MRI that shows nerve root compression.
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6
Q

Management of a Brachial plexus injury?

A

Types

Erb-Duchenne paralysis
damage to C5,6 roots
winged scapula
may be caused by a breech presentation

Klumpke’s paralysis
damage to T1
loss of intrinsic hand muscles
due to traction

There are two prototypical brachial plexus injuries: damage to the upper roots (known as Erb’s palsy) and damage to the lower roots (known as Klumpke’s palsy.

Causes

Common causes of both include trauma, and axillary radiotherapy (often for breast cancer).

Erb’s palsy

Involves the C5-6 nerve roots with corresponding dermatomal sensory loss, and the so-called “waiter’s tip” sign with shoulder adduction, elbow extension, forearm pronation and wrist flexion. It is most typically associated with shoulder dystocia and traumatic childbirth.

Klumpke’s palsy

Involves the C8-T1 nerve roots with corresponding dermatomal sensory loss, and weakness of the intrinsic muscles of the hand. Uncommonly, T1 involvement may also result in an ipsilateral Horner’s syndrome.

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7
Q

Who would you refer this patient to?

A

Neurosurgery-if needed

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8
Q

What are the dermatomes and action responsible?

A

notion

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9
Q

What neurological features can be seen in C5 nerve root compression

A

notion

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10
Q

Brachial plexus nerves and muscles

A

notion

Origin Anterior rami of C5 to T1
Sections of the plexus
Roots, trunks, divisions, cords, branches
Mnemonic:Real Teenagers Drink Cold Beer
Roots
Located in the posterior triangle
Pass between scalenus anterior and medius
Trunks
Located posterior to middle third of clavicle
Upper and middle trunks related superiorly to the subclavian artery
Lower trunk passes over 1st rib posterior to the subclavian artery
Divisions Apex of axilla
Cords Related to axillary artery

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11
Q

How can radiculopathy be differentiated from spine cord compression

A

Patho,

Acute treatment

signs

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12
Q

What is the Prognosis of radiculopathy?

A
  • The prognosis for cervical radiculopathy is favourable: symptoms resolve in most people and without surgical treatment.[6]
  • Surgery also has good results but is indicated in only a minority. It is likely that the attitude of the patient to active rehabilitation is very important for a good result. However, the general prognosis for neck pain is not good and it is often chronic and persistent.
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13
Q

What are the Complications of radiculopathy

A
  • If an intervertebral disc compresses the spinal cord, it can produce myelopathy with weakness, hyperreflexia and neurogenic bowel and bladder dysfunction. There may be associated significant upper limb weakness or numbness as well as pain.
  • Beware of missing serious underlying disease, including malignancy, infections producing abscesses and inflammatory conditions. Always be alert tored flag
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14
Q

What are UMN and LMN signs?

A

LMD dysfunction in the limbs manifests as weakness, atrophy, fasciculations and hyporeflexia. The thighs are often a site of marked fasciculation. Fasciculation can be difficult to distinguish from arterial pulsation, so consider if there is an underlying arterial course before defining twitching movements as fasciculation.

  • Upper motor neurone signs include:
    • Weakness.
    • Spasticity.
    • Hyperreflexia.
    • Positive Babinski’s sign (up-going plantars).
    • Clonus.
    • Positive Hoffman’s reflex (flicking a finger causes adjacent fingers to flex).
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15
Q

What are the yellow flag signs of chronic pain?

A

Identify those at risk of a poor outcome. Yellow flags are indicators suggesting increased risk of progression to long-term distress, disability and pain (red flags are clinical indicators of possible serious underlying conditions).

Biomedical yellow flags: severe pain or increased disability at presentation, previous significant pain episodes, multiple site pain, non-organic signs, iatrogenic factors.

Psychological yellow flags: belief that pain indicates harm, an expectation that passive rather than active treatments are most helpful, fear avoidance behaviour, catastrophic thinking, poor problem-solving ability, passive coping strategies, atypical health beliefs, psychosomatic perceptions, high levels of distress.

Social yellow flags: low expectation of return to work, lack of confidence in performing work activities, heavier work, low levels of control over rate of work, poor work relationships, social dysfunction, medico-legal issues.

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16
Q

What are the chronic pain syndromes

A

Chronic pain is common, you will encounter patients experiencing chronic pain during your careers, no matter which specialty you pursue. Studies have estimated the prevalence of chronic pain in UK adults at anywhere between 13-50%. You may know someone yourself who is living with the daily disease burden of chronic pain.

Chronic pain is more prevalent in some demographic groups, due to a combination of biological, psychological and social factors:

  • Older age groups
  • Co-morbid disease: particularly depression and cardiovascular disease
  • Female gender
  • Socio-economic deprivation
  • Smokers
  • Alcohol dependence
  • Increased BMI

Fibromyalgia,Chronic fatigue syndromes,complex regional pain syndrome

Check MLE

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17
Q

How can power be assessEd?Grading

A

assess ADL, examination against resistance

MRC grading

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18
Q

How can chronic pain be managed?

A

Almost all pain conditions should be managed with a multifactorial approach. Patient and clinicians can easily fall into the cycle of depending on medications alone and gradually up-titrating doses, leading to increased side effects and possible drug dependence. It is important to remember that medication is just “one slice of the pie” in managing a chronic pain condition. Patients should be supported to adopt active coping strategies and take on responsibility to engage with physiotherapy, self-education and CBT as indicated.

nOTION

Non-pharmacological pain management can be divided into psychological interventions and physical:

When considering how psychological interventions work, we need to think back to the concept of total pain. Psychological therapies work by reducing the anxiety, worry and depression that are often caused by or attributed to the experience of pain. They also address ways in which the person thinks about, and manages their pain to help them to learn to live with their pain.

This is an important concept. When dealing with chronic pain we need to be careful not to falsely reassure or enable the patient to believe that analgesia alone will entirely remove their pain. In reality a significant number of people are living with chronic pain and will continue to do so for their entire life. Psychological therapies such as CBT help people to learn how to manage their pain and re-address their ideas and expectations.

When we look at the treatment of pain with medications, there are a wide variety that work in numerous ways. Similarly with the psychological therapies, not all treatments will work for each person. Careful assessment of the pain, and person, will allow you to select the most appropriate option and work from there.

Some people find graded exercise to be very beneficial, others less so. This is a topic currently undergoing significant debate. There is evidence however to show that cognitive behavioural therapy reduces pain intensity, improves function and reduces negative appraisal or “catastrophizing” (Morley, Stephen and Eccleston (1999). Systematic review and meta-analysis of randomized controlled trials of cognitive behavioural therapy and behaviour therapy for chronic pain in adults, excluding headache. Pain. 80. 1-13.) Acceptance and commitment therapy is another kind of therapy that may be suitable for the management of chronic primary pain and is recommended by NICE.

How does a TENS machine work? - Pain gate theory

  • The idea that if you apply pressure (“rub it better”) then pain will be reduced -
  1. C fibres transmit pain from the periphery. C fibres are unmyelinated, A-delta fibres are only minimally myelinated. This makes them comparatively slow.
  2. The projection neurone/ pain gate transmits signals to the sensory cortex
  3. A-beta fibers transmit mechanical stimulation impulses (myelinated - comparatively fast)
  4. Mechanical stimulation activates the inhibitory neurone which is able to inhibit the projection neurone to limit pain.

Summary: mechanicalstimulation inhibits pain signalling

TENs (transcutaneous electrical nerve stimulation) machines are used to manage both acute and chronic pain. They work via sticky pads on the skin that give small electrical currents, feeling like a ‘buzz’ or ‘tingling sensation’. This acts to interrupting painful signals, thus the intensity of the pain is reduced.

They are used for acute pain, such as labour pain. There is little evidence to support their use for chronic pain but some patients may choose to try them, particularly for focal pain such as chronic back paThe WHO pain ladder was initially developed to manage cancer pain and has an emphasis on oral treatments. It is a reliable and safe way to manage pain, but also has flaws in that it was created with oncology patients in mind and leaves out an ever expanding raft of medication and interventions that can be used to treat pain

.

Renal WHO Pain ladder:

Adapted from “Treating Pain in Advanced CKD and Dialysis Patients”, Coalition for Supportive Care for KidneyPatients.

Neuropathic Pain Medication:

Other options used in specialist pain clinics:

  • Local anaesthetic. Often used in nerve blocks or epidurals by anaesthetists with a special interest in pain management
  • Ketamine
  • Clonidine
  • NSAIDs
  • Capsaicin cream (specialist use). The capsaicin (extracted from chillies) cream is rubbed into the painful area and causes interference with the pain signals, in a similar way to TENS machines. Can be used in neuropathic pain management.
  • Facet joint injections for OA spine
  • Spinal cord stimulators. Inserted under the skin and deliver small electrical signals to interrupt pain signals. Below is a spinal x-ray of a patient with a spinal cord stimulator in situ (Chronic Primary Pain Management:

There is no evidence for the use of opioids, anti-epileptics, benzodiazepines, cannabinoids or NSAIDs in chronic primary pain and these may even cause harm.

Some of the harmful effects of chronic opioid use include:

  • Sedation
  • Dizziness
  • Nausea and vomiting
  • Constipation
  • Respiratory depression. Can also increase airway resistance and decrease the patency of the upper airways.
  • Physical dependence and tolerance
  • Delayed gastric emptying
  • Opioid-induced Hyperalgesia
  • Immune suppression
  • Hormonal suppression
  • Muscle rigidity
  • Myoclonus

All patients on long-term opioids should have regular laxatives and a small supply of anti-emetics.

Patches can be used to manage stable, chronic nociceptive pain but are unsuitable for acute or acutely changing pain. They are unsuitable for chronic primary pain, as are all opioids.

Opioid use has also be shown in some studies to be associated with poor self-related quality of life and employment status, increased healthcare use and worse pain (Faculty of Pain Medication).

Important Practice Points Regarding Opioids (Faculty of Pain Management).

  • Patients who do not achieve useful pain relief from opioids within 2-4 weeks are unlikely to gain benefit in the long term.
  • Short-term efficacy does not guarantee long-term efficacy
  • Data regarding improvement in quality of life with long-term opioids use are inconclusive
  • There is no good evidence of dose-response with opioids, beyond doses used in clinical trials (up to 120mg morphine per day). There is no evidence for efficacy of high dose opioids in long term pain.

Pharmacological Management of Chronic Primary Pain:

  • NICE recommends the use of one of the following antidepressants: duloxetine, fluoxetine, paroxetine, citalopram, sertraline or amitriptyline, for people aged 16 years and over to manage chronic primary pain, after a full discussion of the benefits and risks.
  • They have been shown to improve pain, quality of life and psychological distress when compared to placebo drugs.
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19
Q

How can strokes be classified and what is a lacunar stroke?

A

The Oxford Stroke Classification (also known as the Bamford Classification) classifies strokes based on the initial symptoms. A summary is as follows:

The following criteria should be assessed:

  1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
  2. homonymous hemianopia
  3. higher cognitive dysfunction e.g. dysphasia

Total anterior circulation infarcts (TACI, c. 15%)
involves middle and anterior cerebral arteries
all 3 of the above criteria are present

Partial anterior circulation infarcts (PACI, c. 25%)
involves smaller arteries of anterior circulation e.g. upper or lower division of middle cerebral artery
2 of the above criteria are present

Lacunar infarcts (LACI, c. 25%)
involves perforating arteries around the internal capsule, thalamus and basal ganglia
presents with 1 of the following:
1. unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
2. pure sensory stroke.
3. ataxic hemiparesis

Posterior circulation infarcts (POCI, c. 25%)
involves vertebrobasilar arteries
presents with 1 of the following:
1. cerebellar or brainstem syndromes
2. loss of consciousness
3. isolated homonymous hemianopia

Lateral medullary syndrome (posterior inferior cerebellar artery)
aka Wallenberg’s syndrome
ipsilateral: ataxia, nystagmus, dysphagia, facial numbness, cranial nerve palsy e.g. Horner’s
contralateral: limb sensory loss

Weber’s syndrome
ipsilateral III palsy
contralateral weakness

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20
Q

How does cervical spondylosis present?

A

Definition

Cervical spondylosis describes an osteo-degenerative disease of the cervical spine. It is a common, and underdiagnosed, cause of falls in the elderly.

Epidemiology

Prevalence rises with age for men and women and is the highest in the age group between 50-59 years.

Clinical features

Manifestations include:

Neck pain

Radiculopathy due to compression of nerve roots at the site of foraminal exit

Myelopathy, probably due to dynamic stretch of the spinal cord over impinging spinal osteophytes.

On examination, neck pain is accompanied by flaccid upper limb paresis (due to radiculopathy), variable sensory changes (sometimes including the Lhermitte phenomenon), and spastic paraparesis (with variable involvement of the upper limbs depending on the site of the lesion, and degree of radiculopathy).

Bladder and bowel disturbance is rare.

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21
Q

How is cervical spondylosis managed and what are complications

A

Oxford?

22
Q

What is degenerative cervical myelopathy?

A

Degenerative cervical myelopathy (DCM) has a number of risk factors, which include smoking due to its effects on the intervertebral discs, genetics and occupation - those exposing patients to high axial loading [1].

The presentation of DCM is very variable. Early symptoms are often subtle and can vary in severity day to day, making the disease difficult to detect initially. However as a progressive condition, worsening, deteriorating or new symptoms should be a warning sign.

DCM symptoms can include any combination of [1]:
Pain (affecting the neck, upper or lower limbs)
Loss of motor function (loss of digital dexterity, preventing simple tasks such as holding a fork or doing up their shirt buttons, arm or leg weakness/stiffness leading to impaired gait and imbalance
Loss of sensory function causing numbness
Loss of autonomic function (urinary or faecal incontinence and/or impotence) - these can occur and do not necessarily suggest cauda equina syndrome in the absence of other hallmarks of that condition
Hoffman’s sign: is a reflex test to assess for cervical myelopathy. It is performed by gently flicking one finger on a patient’s hand. A positive test results in reflex twitching of the other fingers on the same hand in response to the flick.

The most common symptoms at presentation of DCM are unknown, but in one series 50% of patients were initially incorrectly diagnosed and sometimes treated for carpal tunnel syndrome [2].

An MRI of the cervical spine is the gold standard test where cervical myelopathy is suspected. It may reveal disc degeneration and ligament hypertrophy, with accompanying cord signal change.

All patients with degenerative cervical myelopathy should be urgently referred for assessment by specialist spinal services (neurosurgery or orthopaedic spinal surgery). This is due to the importance of early treatment. The timing of surgery is important, as any existing spinal cord damage can be permanent. Early treatment (within 6 months of diagnosis) offers the best chance of a full recovery but at present, most patients are presenting too late. In one study, patients averaged over 5 appointments before diagnosis, representing >2 years.

Currently, decompressive surgery is the only effective treatment. It has been shown to prevent disease progression. Close observation is an option for mild stable disease, but anything progressive or more severe requires surgery to prevent further deterioration. Physiotherapy should only be initiated by specialist services, as manipulation can cause more spinal cord damage.

23
Q

What are the causes of spinal cord compression?How does it present?

A

Definition

Spinal cord compression (SCC) results from processes that compress or displace arterial, venous, and cerebrospinal fluid spaces, as well as the cord itself.

Clinical features

Cord compression typically presents with acute (or less commonly subacute) upper motor neuron signs and sensory disturbance below the level of the lesion.

Deep and localised back pain is often also present, along with a stabbing radicular sensory disturbance at the level of the lesion. Bladder and bowel involvement is also commonly seen.

Causes

Trauma

Neoplasia (seen in 5-10% of cancer patients, presenting complaint in 20% of these)

Infection (especially TB in at-risk patients)

Disc prolapse

Epidural haematoma

24
Q

How can spinal cord compression be managed?

A

Management

Patient with clinical features suggestive of spinal cord compression or cauda equina syndrome should have an urgent WHOLE spine MRI, with an aim (in appropriate cases) to surgically decompress within 48 hours.

In patients where malignancy is demonstrated on MRI, or in patients where clinical suspicion is high, administration of dexamethasone 16 mg daily in divided doses (with PPI cover) is indicated.

25
Q

What is Cauda Equina Syndrome and how is managed? and present?

A

Cauda equina syndrome (CES) is a rare but serious condition in which the lumbosacral nerve roots that extend below the spinal cord are compressed. It is important to consider CES in any patient who presents with new/worsening lower back pain. Late diagnosis may lead to permanent nerve damage resulting in long term leg weakness and urinary/bowel incontinence.

Causes
the most common cause is a central disc prolapse
this typically occurs at L4/5 or L5/S1
other causes include:
tumours: primary or metastatic
infection: abscess, discitis
trauma
haematoma

It is important to recognise that CES may present in a variety of ways and there is no one symptom/sign that can diagnose nor exclude CES. Possible features include
low back pain
bilateral sciatica
present in around 50% of cases
reduced sensation/pins-and-needles in the perianal area
decreased anal tone
it is good practice to check anal tone in patients with new-onset back pain
however, studies show this has poor sensitivity and specificity for CES
urinary dysfunction
e.g. incontinence, reduced awareness of bladder filling, loss of urge to void
incontinence is a late sign that may indicate irreversible damage

Investigation
urgent MRI

Management
surgical decompression

26
Q

What is the acute management of Stroke?

A

Acute management of ischaemic stroke

Patients should be approached in the DR ABCDE manner.

Airway protection (in patients presenting with depressed consciousness) and aspiration precautions (in patients presenting with swallowing impairment) are very important.

Subsequent stroke management depends on whether the stroke is ischaemic or haemorrhagic. CT head should be performed on arrival to the emergency department to distinguish ischaemic from haemorrhagic stroke.

Alteplase (tissue plasminogen activator) is indicated in patients presenting within 4.5 hours of symptom onset and with no contraindications to thrombolysis (e.g. recent head trauma, GI or intracranial haemorrhage, recent surgery, acceptable BP, platelet count, and INR).
Mechanical Thrombectomy can be performed in patients with anterior circulation strokes within 6 hours of symptom onset, provided that they have a good baseline functional status and lack of significant early infarction on initial CT scan. Mechanical Thrombectomy can also be performed in posterior circulation strokes up to 12 hours after onset.
If hyper-acute treatments are not offered, patients should receive aspirin 300 mg orally once daily for two weeks. If hyper-acute treatments are offered, aspirin is usually started 24 hours after the treatment following a repeat CT Head that excludes any new haemorrhagic stroke.

27
Q

What is the chronic management of stroke?

A

Stroke investigations (post-acute)

Investigations in the post-acute phase aim to further define the cause of the stroke and to quantify vascular risk factors.

Further investigations to determine the cause of the stroke include, for example:

In ischaemic stroke: carotid ultrasound (to identify critical carotid artery stenosis), CT/MR angiography (to identify intracranial and extracranial stenosis), and echocardiogram (if a cardio-embolic source is suspected). In young patients further investigation e.g. a vasculitis screen or thrombophilia screen may be necessary.

In haemorrhagic stroke: serum toxicology screen (sympathomimetic drugs e.g. cocaine are a strong risk factor for haemorrhagic stroke).

Further investigations to quantify vascular risk factors include: serum glucose (all patients with stroke should be screened for diabetes with a fasting plasma glucose or oral glucose tolerance test), serum lipids (to check for raised total cholesterol/LDL cholesterol).

Stroke management (chronic)

The key steps in secondary stroke prevention can be remembered by the mnemonic HALTSS:

Hypertension: studies show there is no benefit in lowering the blood pressure acutely (as this may impair cerebral perfusion) unless there is malignant hypertension (systolic blood pressure >180 mmHg). Anti-hypertensive therapy should, however, be initiated 2 weeks post-stroke.
Antiplatelet therapy: patients should be administered Clopidogrel 75 mg once daily for long-term antiplatelet therapy. In patients with ischaemic stroke secondary to atrial fibrillation, however, warfarin (target INR 2-3. or a direct oral anticoagulant (such as Rivaroxaban or Apixiban) is initiated 2 weeks post-stroke.
Lipid-lowering therapy: patients should be prescribed high dose atorvastatin 20-80 mg once nightly (irrespective of cholesterol level this lowers the risk of repeat stroke).
Tobacco: offer smoking cessation support.
Sugar: patients should be screened for diabetes and managed appropriately.
Surgery: patients with ipsilateral carotid artery stenosis more than 50% should be referred for carotid endarterectomy.
Rehabilitation and supportive management will include an MDT approach with involvement of physiotherapy, occupational therapy, speech and language therapy, and neurorehabiliation.

28
Q

What are the signs and symptoms of multiple sclerosis?

A

NOTION

29
Q

Who is at risk of MS?

A

There are a few factors that increase the risk of developing MS:

  • Age: Most patients are diagnosed with new MS between ages 20-50
  • Gender: MS is 3x more common in females than males
  • Family History: MS is not caused by a single gene, but having a family history of MS slightly increases the risk of developing the disease.
  • Demographics: MS is more common in countries at higher latitudes (furthest away from the equator). This may be related to vitamin D exposure.
30
Q

What is optic neuritis and how does it present?

A

Optic neuritis is an inflammation of the optic nerve (cranial nerve III), reducing it’s ability to carry messages. This leads to a reduction in vision, particularly colour (especially red!) vision. Movement of the eye is often painful as the inflammed and swollen nerve moves. Jenny demonstrates an example of optic neuritis: painful, blurred vision unilaterally, which has gradually developed over several days.

Optic Neuritis is a common presentation of multiple sclerosis, but there are other causes.

Optic neuritis =blurred vision, painful eye movements

Inflammation and de-myelination of the optic nerve

  • Reduced visual acuity, particularly colour vision
  • Pain on eye movement
  • Relative afferent pupillary defect (RAPD) may be present
31
Q

*How can MS be diagnosed?

A

MultipleSclerosis must beMultipleEpisodes of demyelination and damage. These attacks must be disseminated in time and space. i.e. there must be attacks affectingdifferent areas, atdifferent times. Proof of this dissemination may be made clinically or via evidence on MRI scans.

A Clinically Isolated Syndrome is often the first presentation of MS, but proof of dissemination in time and space must be made before we can diagnose Multiple Sclerosis.

MS presents initially with an attack of central nervous system de-myelination. This can happen anywhere in the brain or spine. Signs will be central, not peripheral.

This is a Clinically Isolated Syndrome (CIS), MS is not diagnosed until recurrent attacks that aredisseminated in time and spaceare proven.

Not every person who experiences a CIS will go to develop Multiple Sclerosis. Some people will live their entire lives without ever experiencing another episode.

The symptoms of an attack of CNS de-myelination depend on where the attack is happening. The types of nerve affected will dictate the symptoms that develop, i.e.

  • Inflammation in the sensory nerves of the spinal cord will lead to sensory symptoms below that level in the spine.
  • Inflammation in the balance control parts of the brainstem will lead to loss of the balance and vertigo.

Remember, an attack gradually worsens over a few days-weeks and must last at least 24hours.

The most common types of presentation are:

  • Optic neuritis
  • Transverse myelitis
  • **Brainstem*
32
Q

What are symptoms of transeverse myelitis?

A

Transverse myelitis =leg weakness, sensory changes, bladder/bowel disturbance

An area across (transverse) a section of spinal cord (myel-) that is inflammed (-itis)

  • May affect motor/sensory fibers or both. The types of fibres affected will produce the symptoms experienced by the patient.
  • May present as sensory changes (numbness, tingling) and/or motor changes (loss of power) below the level of the lesion. There is often a sensory level on examination. Signs are CNS not PNS.
  • Bladder, bowel and sexual function can also be involved.
  • The patient may feel a tight band-like sensation at the level of the lesion
33
Q

What is affected in brainstem inflammation as a result of mutiple sclerosis?

A

Brainstem = dizziness, vertigo, double vision

Inflammation to the brainstem or cerebellum. Many of the facial nerves have their origin in the brainstem. The head and neck sensation and power can be affected by inflammation in this area. This is rarer as a presentation of MS.

  • Vertigo and “room-spin” dizziness
  • Painless double vision as nerves controlling eye muscles are affected
  • Facial numbness
  • Dysarthria/Dysphagia

The brainstem co-ordinates the cranial nerves that control eye movement, to keep the eyes moving together smoothly. If it becomes inflamed, it can’t do it’s job properly and the eye movements become disjointed - leading to double vision for the patient as the brain tries to make sense of these disjointed images!

OnABductionof an eye (lateral rectus), we need to rapidly co-ordinateADDuctionof the other eye (medial rectus). To allow this to occur fast enough, a tract called themedial longitudinal fasciculuscrosses over to the contralateral side of the brain stem between the nucleus of the third and sixth cranial nerve. This tract is highlymyelinatedand often affected by MS.

When themedial longitudinal fasciculusis affected, there is a delay inADDuctionof the ipsilateral (same side as affected) eye when the contralateral eyeABducts. The term for this isinternuclear(between cranial nerve nuclei in the brainstem)ophthalmoplegia(eye movement paralysis).

34
Q

How can MS be investigated?

A

Patients presenting with 1 or more episodes suggestive of an inflammatory de-myelination should be investigated for potential MS.

MRI

The 1st line investigation should be an MRI brain and spine to look for evidence of current and old inflammatory plaques.

The ‘classical’ plaques seen in MS are peri-ventricular. These appear on the T2 MRI images as white plaques very close to the ventricles. You can also see plaques in the cerebellum, brainstem or spinal cord. Plaques in different areas can show us evidence ofdissemination in space.

Adding gadolinium contrast to the MRI scan help us see active inflammation vs old inflammation. Active inflammation enhances with gadolinium contrast, old scarring doesn’t. This can show us evidence ofdissemination in time.

  • How can MS be investigated?Patients presenting with 1 or more episodes suggestive of an inflammatory de-myelination should be investigated for potential MS.MRIThe 1st line investigation should be an MRI brain and spine to look for evidence of current and old inflammatory plaques.The ‘classical’ plaques seen in MS are peri-ventricular. These appear on the T2 MRI images as white plaques very close to the ventricles. You can also see plaques in the cerebellum, brainstem or spinal cord. Plaques in different areas can show us evidence ofdissemination in space.Adding gadolinium contrast to the MRI scan help us see active inflammation vs old inflammation. Active inflammation enhances with gadolinium contrast, old scarring doesn’t. This can show us evidence ofdissemination in time.Oligoclonal bands:These are evidence of inflammation and immunoglobulin synthesis. If they are foundonlyin the cerebrospinal fluid andnotin the blood then this suggests inflammationconfinedto the central nervous system not the rest of the body. CSF oligoclonal bands are found in MS, but also in other CNS inflammatory conditions such as encephalitis, sarcoidosis, lupus etc. This test issupportiveof an MS diagnosis ( if in keeping with a matching clinical history) but isnot specific.The presence of oligoclonal bands in suspected MS suggests longer-term inflammation so is sometimes used as evidence supportive ofdissemination in time.Rule out other differential diagnosis:If the presentation is atypical, or another cause is suspected, then tests may be performed to look for this. These may include a general bloods screen, specific autoantibodies, infection screens. These will likely be guided by an experienced neurologist based on the patient’s clinical presentation.Examples of some of the investigationsMRI Brain Report:MRI Spine report:CSF Oligoclonal Bands:Serum Oligoclonal Bands:Routine Blood Screen:
35
Q

What is the diagnostic criteria for MS?

A

As we have discussed, to make a diagnosis of multiple sclerosis we must have evidence of multiple attacks.

These must be spread out intimeandspace.

For this reason recurrent attacks of symptoms affecting the exact same spot of the brain does not constitute MS.

Similarly, a set of symptoms which affects many areas of the brain acutely and simultaneously does not constitute MS.

Attacks must happendisseminated in time and space.

Some attacks may be sub-clinical. This means they will show up on an MRI scan but may not have caused any symptoms for the patient.

The McDonald criteria are used to guide this diagnosis.

You don’t need to memorise the entire guidelines, the take-away message is to assess what evidence you have and what evidence you still to provedissemination in time or space.

Think about the clinical evidence of attacks that you have, and how many lesions are visible on the MRI images.

Sometimes there is not enough evidence to make a firm diagnosis of MS. This means the doctor and the patient will have to adopt a “watch and wait” approach to see if other attacks will occur. The patient must be educated about the signs to look out for. This can be a stressful and anxiety inducing experience for a patient.

36
Q

What are the different patterns of MS progression?

A

Relapsing-Remitting disease is the most common (85%) course of disease in the initial phases. This is a disease characterised by relapses and remission, with gradually reducing functional reserve after an attack.

As time progresses and the disease reaches it’s later stages this may evolve into secondary progressive disease, a gradual loss of function with no distinct relapses and remission.

Some people (15%) are diagnosed with primary progressive MS at the outset of disease. This is gradually progressive symptoms from the outset. This is more common in male MS patients.

Benign MS is rare, characterised by relapses and remissions with no disease progression.

MS progression tends to follow certain ‘patterns’.

Patients might be very concerned about what type of MS they have, but it is not easy to predict exactly how their disease will progress. Early education, supportive care and a discussion about disease-modifying treatments should be available to all patients.

37
Q

What is a relapse?

A

Multiple sclerosis progresses over time.

Relapsing-Remitting MS:Deterioration occurs in ‘relapses’, which then totally or partially recover.

Primary or Secondary Progressive MS:Deterioration happens gradually, sometimes with relapses as well. There is an accumulation of neurological disability without remission between episodes.

A remission of MS is defined as:

  • A neurological disturbance
  • Lasts longer than 24hours
  • Happens after more than 30 days of clinical stability
38
Q

How to assess an MS relapse?

A

The first step of assessment for MS relapse should always be torule out infection

Infection or fevers can lead to a temporary worsening of existing MS symptoms, as opposed to a new relapse with a new episode of inflammatory de-myelination.

The work-up for a possible MS relapse should always include looking for any signs of infection, particularly a UTI:

  • Thorough history and examination
  • Observations
  • Urine dipstick +/- culture
  • CXray if any respiratory symptoms/cough
  • Standard blood tests: FBC, U&Es, CRP

As well as infection, stress/heat/over exertion can also lead to a symptom deterioration. It is important to rule these factors out first, before jumping in to starting treatement.

An MRI can be useful to show evidence of a relapse if there is clinical uncertainty. Anewlesion, whichenhanceswith gadolinium contrast (showing active inflammation) is suggestive of an MS relapse. MRI is not always needed if clinical certainty is high.

39
Q

How can MS be treated?

A

The aim of treatment for a MS relapse is to speed up recovery time. Treating an MS relapse does not impact on future disability or reduced risk of future relapses.

We treat relapses that cause symptoms that impact on a patient’s ability to function and perform their activities of daily living.

An MS relapse is treated with high dose steroids - to suppress the immune system and inflammation. This is why ruling out an infection first is so important, you don’t want to suppress the immune system of someone trying to fight off an infection!

MS relapses are treated with high dose IV or oral prednisolone for a few days.

DMTs aim to influence the progression of the disease. They do not cure the underlying disease itself. The aim is to:

  • Reduced the frequency of relapses
  • Reduce the progression of neurodisability

DMTs are givenearly,when the disease is in therelapsing-remittingphase.

paTIENT CHOICE

  • Beta interferon
  • fingolimod
  • Alemtuzumab

The decision about when and what disease modifying treatment to start is not easy. There are different options available. This will usually be a shared decision between a specialist consultant and the patient.

You don’t need to memorise all of the medications available, the guidelines are changing frequentlyas the research progresses. It is enough to know that different options are available, and that these are a balancing act between efficacy and safety.

DMTs suppress the immune system. The stronger the DMT is, the more effective it is at reducing relapses. However, the risk of infections goes up. The condition that gets neurologists most worried is PML.

40
Q

What is major risk of giving disease modifying therapy?

A

Progressive Multifocal Leukoencephalopathy (PML)

This is a rare condition, you don’t need to know everything about it.

Just be aware that PML is the big risk that neurologists think about when using DMTs, especially Natalizumab. The strongest DMTs carry the greatest risk.

PML is caused by reactivation of the JC virus in the CNS. Much of the general population has already been exposed to the JC virus and carries it in an inactive form. When the immune system is suppressed by DMTs, this virus can reactivate in the brain and cause significant neurological problems and even death. MS patients will have blood tests to assess the amount of JC virus antibody in their blood. This can guide treatment decisions.

41
Q

What are symptoms of MS and how can these be managed?

A

Fatigue:The degree of fatigue in MS is can be overwhelming and disabling

  • Cooling, Pacing activities, CBT, Mindfullness, Amantadine

Mood:Depression is common in MS

  • CBT, SSRIs, Duloxetine

Cognition:Cognition deteriorates as disease becomes advanced

  • Social support, rule out sleep issues/pain/depression

Spasticity:This can lead to pain and discomfort

  • Physiotherapy, Baclofen, BoTox

Pain:Typically neuropathic type pain

  • CBT, Amitriptyline, Gabapentin, Pregabalin

Neurogenic bladder issues:Urinary frequency, urgency, nocturia. Frequent UTIs.

  • Fluid intake control, regimented toilet regime, Oxybutinin, BoTox injection, intermittent self-catherterisation

Constipation:Difficulty opening bowels, or mobilising to toilet

  • Good diet and fluid, regular laxatives, bowel care, assistedevacuation, good hygiene

Other symptoms to be aware of:

  • Lhermitte’s symptom: ‘Electric shock’ felt down back of spine on neck flexion
  • Urthoff phenomenon:Symptoms worsening in the heat e.g. hot bath
42
Q

What members of the MDT is involved in the care of a patient with MS?

A

Many teams are involved in the care of an MS patient.

Early contact and support from an MS specialist nurse can have a huge impact on patient education and care.

Educating the patient for possible symptoms and sign-posting to appropraite services is a vital part of long term MS care.

43
Q

What Future treatment options are likely?

A

The last 30 years have been revolutionary for MS treatment. Interferon beta 1a was the first DMT to be approved for use in MS in 1993. Since then more and more DMTs have been researched and approved to influence and slow down the progression of the disease. This research remains ongoing, with more drugs in the pipeline.

What does the future look like for MS treatment?

The future of MS treatment could hold potential cures, ways to reverse the damage done or halt the disease in it’s primary/secondary progressive phases.

Researchers are looking into the role of genetics, vitamin D and lifestyle factors in predicting and preventing the onset of MS.

Drug approval process

Research into MS is constantly ongoing. researchers are searching for more effective biological agents to modify the course of the disease. New drugs are invented, but there is a long journey before they can start being used to treat patients.

For a new drug to be available to the public on the NHS it must pass several stages

It must be proven to beeffective, safe and cost effective

Below is a simplification showing the journey a new drug must pass before being available to the public on the NHS

44
Q

What is the nihss SCORE?

A

The NIH Stroke Scale (NIHSS) is a scoring system out of 42, which has been designed as a predictive score of clinical outcome in stroke.
This scoring system is completed on initial assessment of a patient with suspected stroke. It is important for the consideration of thrombolysis and clinical outcome.

A score < 4 is associated with a good clinical outcome. A high score (> 22) indicates a significant proportion of the brain is affected by ischaemia, and as such, there is higher risk of cerebral haemorrhage with thrombolysis. A score ≥ 26 is often considered a contraindication to thrombolysis.

45
Q

Contraindications for thrombolysis

A

Contraindications to thrombolysis:

Absolute

  • Previous intracranial haemorrhage
  • Seizure at onset of stroke
  • Intracranial neoplasm
  • Suspected subarachnoid haemorrhage
  • Stroke or traumatic brain injury in preceding 3 months
  • Lumbar puncture in preceding 7 days
  • Gastrointestinal haemorrhage in preceding 3 weeks
  • Active bleeding
  • Pregnancy
  • Oesophageal varices
  • Uncontrolled hypertension >200/120mmHg

relative

  • Concurrent anticoagulation (INR >1.7)
  • Haemorrhagic diathesis
  • Active diabetic haemorrhagic retinopathy
  • Suspected intracardiac thrombus
  • Major surgery / trauma in the preceding 2 weeks
46
Q

When is a thrombectomy done?

A

Mechanical thrombectomy is an exciting new treatment option for patients with an acute ischaemic stroke. NICE incorporated recommendations into their 2019 guidelines. It is important to remember the significant resources and senior personnel to provide such a service 24 hours a day. NICE recommend that all decisions about thrombectomy take into account a patient’s overall clinical status:
NICE recommend a pre-stroke functional status of less than 3 on the modified Rankin scale and a score of more than 5 on the National Institutes of Health Stroke Scale (NIHSS)

Offer thrombectomy as soon as possible and within 6 hours of symptom onset, together with intravenous thrombolysis (if within 4.5 hours), to people who have:
acute ischaemic stroke and
confirmed occlusion of the proximal anterior circulation demonstrated by computed tomographic angiography (CTA) or magnetic resonance angiography (MRA)

Offer thrombectomy as soon as possible to people who were last known to be well between 6 hours and 24 hours previously (including wake-up strokes):
confirmed occlusion of the proximal anterior circulation demonstrated by CTA or MRA and
if there is the potential to salvage brain tissue, as shown by imaging such as CT perfusion or diffusion-weighted MRI sequences showing limited infarct core volume

Consider thrombectomy together with intravenous thrombolysis (if within 4.5 hours) as soon as possible for people last known to be well up to 24 hours previously (including wake-up strokes):
who have acute ischaemic stroke and confirmed occlusion of the proximal posterior circulation (that is, basilar or posterior cerebral artery) demonstrated by CTA or MRA and
if there is the potential to salvage brain tissue, as shown by imaging such as CT perfusion or diffusion-weighted MRI sequences showing limited infarct core volume

47
Q

What advice would you give them regarding driving?

A

stroke or TIA: 1 month off driving, may not need to inform DVLA if no residual neurological deficit
multiple TIAs over short period of times: 3 months off driving and inform DVLA

chronic neurological disorders e.g. multiple sclerosis, motor neuron disease: DVLA should be informed, complete PK1 form (application for driving licence holders state of health)

48
Q

When is carotid endartectomy done?

A

patients with ipsilateral carotid artery stenosis more than 50% should be referred for carotid endarterectomy.

49
Q

What antibodies are tested for in MS?

A

Antibody testing

Useful in the work-up of MS if an alternative demyelinating condition is suspected (e.g. Neuromyelitis optica). Both AQP4 and myelin oligodendrocyte glycoprotein (MOG) antibodies are associated with NMOSD.

50
Q

Read mono and poly neuropathies plus intracranial bleeds

A

Oxford

51
Q

How many recover after stroke?

A

Check

52
Q

Scoring systems used in stroke?

A

Fast
ROISER score
Stroke scale