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year 4 CDM 2 > Case 18: Functional neurology > Flashcards

Case 18: Functional neurology Flashcards

1
Q

Functional neurology statistics

A
  • 10% of outpatient referrals and 10% of admissions
  • Present with pain, fatigue, sensory symptoms, seizures, movement disorders (tremors, spasms, jerks, tics, dystonia), weakness, visual loss, gait disorders, cognitive decline
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2
Q

Functional disorders: types

A
  • Cardiology - non-cardiac chest pain
  • Gastroenterology - IBS
  • Respiratory - chronic cough, brittle asthma
  • Renal - recurrent loin pain
  • Surgery - chronic abdo or pelvic pain
  • Rheumatology - fibromylagia
  • ID - chronic fatigue syndrome
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3
Q

Non epileptic attacks (dissociative attacks)

A
  • Can co-exist with epilepsy
  • Can end up intubated and ventilated due to ‘non-epileptic status’
  • Tend to have a prodrome but takes effort for patient to describe
  • Often a sense of feeling “unreal” and “detached” or even a sense of rising panic
  • Often variable in presentation (but not always)
  • Tend to have an awareness but may be muffled or from a distance
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4
Q

NEA symptoms

A
  • Before: Long prodrome (often the sensation of feeling detached or unreal), rapid breathing in run up to attack
  • During the attack: Conscious retained, violent thrashing or side to side head movement. May fall down and lie still, resisting eye opening (indicates a degree of awareness)
  • Recovery: orientated rapidly, may feel upset or emotional
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5
Q

How to differentiate non-epileptic attacks from seizures

A
  • NEA: patients may fall down and lie still (particularly suspicious if >5mins). Attacks can go on for >5 minutes without hypoxic or metabolic consequences (unusual in epilepsy but people are poor judges of time)
  • Helpful clues to NEA’s: gradual onset, violent thrashing or side to side head movement, hip thrusting, resisting eye opening. Rapid breathing particularly in the run up to an attack
  • Helpful to know if there is a tonic phase
  • Not so helpful: incontinence (seen in all 3), tongue biting (unless severe and on the side of the tongue then epilepsy). Self injury and response to pain during attacks (can be severe in NEA and epilepsy)
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6
Q

How epileptic seizures present: unusual features

A
  • Primary generalised seizure: dont get an aura
  • Secondary generalised tonic-clonic seizures: have a focal onset before generalising
  • Temporal Lobe epilepsy often have a brief prodrome which is always the same, can have impaired awareness
  • Focal: can have retained awareness, prodrome same every time
  • Frontal seizures: can be unusual but in the same way each time
  • Generalised: always have impaired awareness
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7
Q

Functional presentations

A
  • Weakness - gradual onset or sudden, can present like a stroke (hemiplegic)
  • Sensory loss “split down the middle” (but can be due to a thalamic lesion otherwise functional); limb sensory symptoms that stop at the groin or shoulder
  • Tremor - variable and entrainable
  • Dystonia ‘(fixed muscle contraction) can be very bizarre with secondary skin changes, very disabling
  • Gait disorders: dragging leg, crouching gait, tightrope gait without falling
  • Cognitive decline although can usually give a very clear account of them
  • Visual loss; tubular fields (restricted fields) or blindness with preserved pupil reflexes and optico-kinetic nystagmus i.e. eyes respond to stimuli even though they say they cant see
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8
Q

How to describe a functional diagnosis to a patient

A
  • The underlying structure is working fine but the function is not
  • Use example of migraine where patient has really severe symptoms but when you scan the brain nothing comes up
  • ‘I do not think you are making up your symptoms’
  • Can show Hoovers sign
  • ‘This is very common and is seen a lot’
  • ‘The hardware is good but the software is not’
  • Not helpful to focus on mental health if they came in with physical issues
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9
Q

Seizure types

A
  • Focal: aware (simple), awareness impaired (complex)
  • Focal: motor onset, non-motor onset (sensory, autonomic, psychic)
  • Focal can progress to generalised
  • Generalised: tonic clonic or absence. Other motor seizures include tonic, clonic, myoclonic and atonic
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10
Q

Absence seizures

A
  • Last 1s, eyes flutter, occur in paediatrics
  • Cant develop absence seizures in adulthood but might be retained from childhood
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11
Q

Fits, faints and funny turns

A
  • Changes in awareness or consciousness
  • Faint: lack of blood supply to the brain (low blood pressure) due to cardiac disturbance
  • Seizure: electrical disturbance
  • NEA: psychological disturbance (in part) causing physical symptoms, transient disconnection of mind from body
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12
Q

Generalised seizures

A
  • Seizure which affects the whole brain (both hemispheres)
  • Loss of consciousness with no awareness
  • No prodrome
  • Patient gives little history
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13
Q

Focal seizures

A
  • Seizure activity starts in one area of the brain
  • Tend to last minute or two
  • Will have prodrome, may have retained awareness
  • Symptoms dependent on brain area
  • Focal seizure: have structural abnormality until proven otherwise (need a scan)
  • Retained awareness: sensory, autonomic, motor, psychic. Can progress to impaired awareness
  • Can have focal seizures with impaired awareness - these can progress to generalised seizures
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14
Q

Loss of conscious: feeling before

A
  • Syncope: may feel hot, sweaty, blurred vision. 3 P’s (posture- standing upright, precipitant i.e. taking blood, prodrome)
  • Seizure: generalised (usually no warning). Warning symptoms usually represent the focal seizure starting
  • NEA; tend to have warning i.e. felt like they were hearing things from a distance. Can be at rest or triggered. Can feel disconnected: ‘weird’, ‘spaced out’ called dissociation
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15
Q

Loss of conscious: during

A
  • Not that helpful
  • In generalised seizures may groan due to tonic contraction of diaphragm
  • NEA: retained awareness, can have feeling of ‘dissociation’ or watching from the outside’
  • If the patient can describe the attack it probably isn’t a generalised seizure
  • Seconds: think syncope (tend to twitch and jerk a bit)
  • 1-2 minutes: think seizure
  • 10+ minutes: think Non epileptic attack disorder (NEAD) or catastrophic status epilepticus (obvious)
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16
Q

Cardiac syncope

A
  • Before:Onsetduringexertion. Sudden onset, with little warning. Usually no prodrome may have chest pain/palpitation
  • During:Brief loss of consciousness, in keeping with syncope. Few seconds usually no movement, incontinence and tongue biting is rare
  • After:Rapid recovery after collapse, in keeping with syncope.
  • Investigations: ECG, lying and standing BP, full set of bloods
  • Refer urgently to cardiology
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17
Q

Blackouts: when to refer urgently to cardiology (within 24hr)

A
  • An ECG abnormality.
  • Heart failure (history or physical signs).
  • TLoC during exertion.
  • Family history of sudden cardiac death in people aged younger than 40years and/or an inherited cardiac condition.
  • New or unexplained breathlessness.
  • A heart murmur
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18
Q

Differentiating NEA: After

A
  • Syncope: orientated rapidly, feel shaky and rubbish
  • Seizure: not right for ages, confused, drowsy, aggressive, achy. May break bones during, feel like the have run a marathon. May take a while to recognise people
  • NEA: orientated rapidly, upset, emotional. Can recognise people immediately
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19
Q

Epilepsy specific symptoms

A
  • Tongue biting: tip of the tongue in NEA, sides in epilepsy
  • Urinary incontinence: can occur in all
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20
Q

Investigations: blackouts and funny terms

A
  • Clinical diagnosis
  • ECG, some people get a CT especially if focal onset
  • Rarely EEG
  • Ask for witness history: ask what happened in the first 10s and so on.
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21
Q

Seizure summary

A
  • Triggered: rare, if they have aura it will be the focal onset of the seizure
  • Before: may have focal onset- deja vu, olfactory/visual hallucinations
  • During: tonic-clonic, focal, absence. Usually 1-2 minutes
  • After: post ictal confusion, Todd’s paresis, drowsy, aggression. Lasts minutes-hours, groggy confused not recognising location/people. Can be aggressive/agitated
  • Duration: usually 1-2 minutes <5 minutes
  • Features: lateral tongue biting, urinary incontinence, stereotyped
  • Investigations: raised lactate, raised WCC, EEG abnormal during
22
Q

Syncope summary

A
  • Triggered: often, hot/crowded, standing up
  • Before: lightheaded, dizzy, vision/hearing receding, pale, clammy, palpitations
  • During: often have myoclonic jerks, few seconds up to 2mins
  • After: groggy but orientated, fast recovery (10-15mins). Recognise location and people
  • Duration: usually <1 minute
  • Features: urinary incontinence unlikely, often prodromal
  • Investigation: L/S BP may show orthostatic hypotension, check ECG
23
Q

Dissociative attack summary

A
  • Triggered: sometimes stress/anxiety
  • Before: anxiety symptoms (sweating, palpitations, paraesthesia), Dissociation (spaced out, disconnected feelings), panic attack
  • During: retained awareness ‘dissociation,’ variable movements, crescendo-ing. May be prolonged
  • After: usually good recovery but may be drowsy/distressed
  • Features: resist eye opening, asynchronous movement, pelvic thrusting
  • Investigation: normal bloods, normal EEG during event, ECG
  • Need to inform DVLA cant drive, refer to first fit clinic
  • Manage similar to epileptic seizure as likely differential
24
Q

Dissociative non-epileptic attack movement

A
  • Less stereotyped. May wax and wane. Axial and head movements may be present. Eyes may be shut, resist opening. May vocalise.
  • Tongue biting more likely the tip
25
Q

Chronic pain

A
  • Pain that lasts longer than 3 months persisting beyond the expected healing time for an episode of tissue damage.
  • Types of chronic pain: nociceptive, neuropathic, nociplastic
  • Pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors
  • Sometimes cant be explained by an organic disease alternatively there is an organic disease but the pain is a lot more severe than is usually expected this is ‘Nociplastic’
  • Also called: ‘functional pain syndromes’ or ‘pain sensitisation syndromes’ when Nociplastic
26
Q

Causes of Nociplastic chronic pain (1/2)

A
  • Central Sensitisation: increased responsiveness of nociceptors in the central nervous system. Previous painful experiences increase this sensitisation process. This can lead to usually non-painful stimuli (e.g. gut peristalsis in IBS) being processed as painful.
  • Reduced negative feedback: Reduced negative inhibition via the descending pain pathways. Because of the close ties with the cortex and limbic system, depression/anxiety/stress inhibit this system, leading to reduced pain inhibition.
27
Q

Causes of Nociplastic chronic pain (2/2)

A
  • Somatisation: Manifestation of psychological distress as physical pain or symptoms (similar to stress being felt as a headache). Becomes pathological when prolonged and distressing.
  • Chronic nociceptic or neuropathic pain can lead to nociplastic pain: neuromodulation can result in increased nociplastic pain
28
Q

Different causes of chronic pain

A
  • Nociceptive pain: Usually due to an organic disease. Pain that is triggered by stimuli that damage or threaten tissues. The most common of these is musculoskeletal e.g. osteoarthritis. This also includes cancer pain, visceral pain etc.
  • Neuropathic pain: Due to pathology or pathological response of sensory nervous system e.g. peripheral neuropathy, MS, post-herpetic pain etc.
  • Nociplastic pain: Caused by abnormal pain processing, even when no physical/organic damage has occurred to our tissues or nerves.
  • Can experience more than one type of pain at once
29
Q

Somatic and visceral pain

A
  • Somatic (skin, muscles, bone): Aching, throbbing, sharp, stinging. Often triggered by movement/palpation. Usually well-localised - patient often can point to the source of the pain with 1 finger. Examples; fractures, osteoarthritis, muscle strain
  • Visceral (organs)Aching, cramping, pressure. Often poorly localised, pain can be referred. Patient points to a generalised area of pain. Example: gastroenteritis, biliary colic, angina
30
Q

Central pain and Neuropathic pain

A
  • Central pain = Originating from the central nervous system, varied character. Can be similar to neuropathic. Often constant pain, worsened by movements. May be associated with paraesthesia or hypersensitivity. Examples: Post-stroke pain, MS pain, fibromyalgia
  • Neuropathic: Burning, coldness, tingling, electric-shocks. Can be localised or referred. Patients often find it hard to describe this type of pain. May be in a ‘length-dependent’ or dermatome distribution. Examples: peripheral neuropathy, local nerve damage
31
Q

Chronic pain risk factors

A
  • Older age groups
  • Co-morbid disease: particularly depression and cardiovascular disease
  • Female gender
  • Socio-economic deprivation
  • Smokers
  • Alcohol dependence
  • Increased BMI
  • Acutely painful experience: i.e. post operative pain, acute illness or a traumatic accident. Acute pain being poorly controlled or associated with psychological distress increases the risk of it becoming chronic
32
Q

Pain transmission and inhibition

A
  • Experience of pain is modulated in the brain either heightened or inhibited
  • Ascending pain pathway: transmits pain perception
  • Descending pain pathway: inhibits pain perception. Endorphins like dopamine, adrenaline and Serotonin inhibit the pain response
  • The ascending pathway feeds into our sensory and emotional processing centres and gives feedback to the PAG. The PAG then sends out negative pain modulation to reduce the response
33
Q

Ascending pain pathway

A
  • Pain travels from the peripheral sensory nerves up the spinothalamic tract to the brain.
  • cortex (helps localise the pain)
  • midbrain (general arousal)
  • the limbic system (emotional processing)
  • Periaqueductal gray or PAG (feeds into the inhibitory descending pathway)
34
Q

Descending pain pathways

A
  • Reduces sensation of pain
  • Modulated by PAG (Periadequeductal gray) which receives input from the limbic system. Releases neurotransmitters which reduce the pain sensation
  • Neurotransmitters: GABA, Exogenous endorphins (act on opioid receptors), Serotonin, Noradrenaline
  • Chronic pain is more common in anxiety/depression/stress: as the descending pain pathway is closely associated with the limbic system
35
Q

Drugs which work on the pain response

A
  • Reduce ascending pain, facilitate descending modulators
  • Facilitates descending modulation: Gabapentin, Pregabalin, Amitriptyline, Duloxetine, Tramadol
  • Reduce ascending pain: NSAID’s, Opioids, Lidocain, Capsaicin
36
Q

Chronic pain investigations

A
  • Need to consider the bio-psycho-social approach
  • Consider red flags: signs of serious organic disease i.e. PR bleeding in abdo pain
37
Q

Psychological risk factors for developing chronic pain following a painful event

A
  • maladaptive health behaviours
  • passive coping strategies
  • anxiety/ depression
  • stress and unresolved anger
38
Q

Chronic pain: yellow flags

A
  • Maladaptive health behaviours
  • Adopting ‘passive’ rather than ‘active’ coping strategies
  • Anxiety, Depression and social isolation]
  • Financial insecurity
  • Lack of social support or ‘over-protective’ caregivers
  • Ongoing litigation related to original pain/injury source
  • Job insecurity
  • Loss of hobby and ‘sense of self’
  • Unresolved anger
  • Poor job satisfaction or extended sick leave
39
Q

Maladaptive health beliefs and behaviours

A
  • The belief that feeling pain means harm is occurring
  • Fear-avoidance of activities due to fear of pain/re-injury
  • Catastrophic thinking
  • Reliance on passive coping strategies (e.g. drugs and rest) rather than active (e.g. physiotherpay)
  • Low expectations of recovery
  • Adopting “the sick role”
40
Q

What groups are more likely to develop chronic pain

A

Older age, female, comorbid disease, socioeconomic deprivation, smokers, alcohol dependence, high BMI.

41
Q

Fibromyalgia

A
  • Causes chronic widespread pain affects 2% of the population. More common in women than men. Affects an age but particularly 25-55
  • Affects joints and muscles, is chronic (lasting >3 months) and fluctuates day to day
  • Associated with conditions like depression and IBS
  • Associated with fatigue, poor sleep and poor concentration
  • > 11/18 tender points is supportive of fibromyalgia diagnosis
  • Risk factor for fibromyalgia: rheumatological disease i.e. OA or RA
42
Q

Systemic symptoms of fibromyalgia

A
  • Central: MH (depression/anxiety), poor sleep, poor concentration, poor memory
  • Urogenital: urinary urgency, irritable bladder, chronic pelvic pain
  • Systemic: fatigue, weight gain, sensitive to hot/cold
  • Headaches: migraine, tension
  • TMJ dysfunction
  • GI: IBS, Nausea, GORD, Oesophageal dysfunction
  • Neurological: Vertigo, Blurred vision, Paraesthesia
43
Q

Fibromyalgia investigations

A
  • Other than pain examination will be normal (i.e. no swelling/erythema/restriction of passive movement) blood tests and imaging will be normal
  • Bloods: FBC, U&E’s, Bone panel, TFTs, CRP, ESR
  • If suspect differential diagnosis: RF, ANA, CK, specific autoantibodies
44
Q

Fibromyalgia differential diagnosis’s

A
  • Osteoarthritis - localised pain, creptius, restricted movement, joint effusion, finger deformity (x-ray)
  • RA - morning stiffness >30 minutes, hot/swollen/red joints, joint deformity, associated skin/lungs/eye signs - RF, anti-CCP, ESR
  • Connective tissue disease i.e. lupus, scleroderma - Raynauld’s phenomena, rashes, joint swelling, weight loss, systemic disease etc - ANA, ESR, specific antibodies i.e. anti-dsDNA
  • PMR - shoulder and pelvic girdle pain, age >50, morning stiffness >30 mins - ESR, CRP
  • Myopathies - Weakness in proximal muscles, systemic disease, FH, statins - CK, U&E’s, bone profile
45
Q

Chronic fatigue syndrome

A
  • Fatigue which is disabling in frequency and severity - tends to be post-exertional
  • Long standing fatigue (4+ months) causing a significant reduction in activity levels
  • Symptoms are not explained by an alternative diagnosis i.e. depression, arthritis, malignancy etc
  • May present at the same time as IBS, migraine and fibromyalgia
  • Often has a ‘triggering event’ like EBV, other viral infections and vaccinations at times of stress/exertion
  • No known cause, suggests neuroinflammatory and neuroendocrine involvement
  • Investigations: routine ‘Tired all the Time’ (TATT)
46
Q

Chronic fatigue syndrome (CFS) criteria

A
  • Present for >4 months
  • New or clear onset
  • Not explained by anything else (including severe obesity BMI >40)
  • Causes significant reduction in activity level
  • Classically post-exertional (typically delayed onset, and lasts >24 hours)
47
Q

CFS is associated with at least one of

A
  • Difficulty sleeping
  • Widespread muscle/joint pain
  • Cognitive impairment i.e. poor memory, word-finding difficulties, poor concentration
  • Ongoing flu-like symptoms: malaise, painful lymph nodes, sore throat, headaches
    -Dizziness/nausea/palpitations/orthostatic intolerance
48
Q

CFS investigations

A
  • Bloods: FBC, U&E, LFT, TFT, CRP/ESR, HbA1c, IgA anti-tissue transglutaminase (anti-ttg) - coeliac disease can cause fatigue without GI symptoms
  • If suggestive history: bone panel/myeloma screen, vitamin D, EBV/CMV, Lyme serology, HIV/Hepatitis
49
Q

CFS management

A
  • May be able to live independently or be fully bed bound
  • Previously recommended CBT and graded exercise therapy
  • Focused on coping not curative therapies
  • Taught pacing techniques to avoid over exertion
  • Support patient to understand the disease and find adaptions to cope
50
Q

Complex regional pain syndrome (CRPS)

A
  • Very rare
  • Affects a distal limb after an event like fracture, surgery or trauma
  • Area develops chronic severe and debilitating pain in excess of what is expected from the original injury
  • Symptoms start within 1 month of the injury
  • Due to damage from either 1 major nerve or to the small sensory and autonomic nerves in an area.
  • Often clinical signs- usually affects a distal limb
  • Amputation can lead to phantom limb syndrome

year 4 CDM 2 (39 decks)

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