Flashcards in Nervous system Dan Deck (89):
How is Post herpetic neuralgia defined?
Pain lasting more than 4 weeks after zoster vesicles healed
older pts are more at risk of Post herpetic neuralgia
almost 50% of over 60s
can be disabling - tends to be more severe and longer lasting in older age
worth immunising older people to reduce zoster risk
vaccine reduces the incidence of both zoster reactivation and post herpetic neuralgia
Pain of Post herpetic neuralgia is worsended with stress
has an autonomic component – worse when stressed, eases with relaxation
compression can relieve pain of Post herpetic neuralgia even when allodynia present
Post herpetic neuralgia can cause anaesthesia dolorosa
sensory loss in area of pain
Treatment ladder for Post herpetic neuralgia
Simple analgesia can be helpful esp if mild – paracetamol, NSAIDs
Topical capsaicin 0.025-0.077% applied 3-4x per day is effective but can cause burning pain and hyperalgesia
Topical 5% lignocaine patches
Amitryptaline (TCA) 70mg daily – effective in 60% - cholinergic AEs; sometimes other TCAs e.g. nortryptaline
Gabapentin, Pregabalin (GABA analogues) – at least as effective as the antidepressants above but fewer side effects
Opioids – oxycodone, tramadol – try after the above
Clonidine (central α2 agonist)
Baclofen (GABA analogue, antispasmodic)
Intrathecal methylprednisolone weekly
Spinal cord stimulators
Refer to pain clinic or neurologist
treating zoster with antivirals up to 10 days after onset can reduce risk of and severity of Post herpetic neuralgia
Can reduce pain/severity and duration but not incidence of PHN
but works best in first 72 hrs
TCS during zoster reduce risk of and severity of Post herpetic neuralgia
acupuncture is proven to help Post herpetic neuralgia
Surgical techniques are last line but effective treatment for Post herpetic neuralgia
What are causes of neuropathic ulcers?
T2 Diabetes – vast majority
Tabes dorsalis (tertiary neurosyphylis)
Spinal cord injury
Hereditary sensory and autonomic neuropathies
In neuropathic ulcers cellulitis or palpable bone using a wound probe indicate high risk of osteomyelitis and the foot should be X-rayed
can show osteomyelitis, foreign body, gas in tissues or bony abnormality
How do you care for neuropathic feet to prevent ulcers?
Inspect feet daily and keep clean and dry
Have regular podiatry for callous removal etc
Should be taught correct toe nail cutting
Need shoes with round or square toe box and low heel to prevent excess pressure on forefoot
Urea products may help callus
Stop smoking, control HTN and diabetes, may need aspirin
What is total contact casting (TCC)?
a way to make a plaster of paris boot that completely encompasses the foot and lower leg and redistributes pressure to completely off-load the usual pressure points
boots applied weekly initially then every 3 weeks
How do you manage established neuropathic ulcers?
Dressing with hydrogel or hydrocolloid dressings (hold a lot of water)
Offload pressure eg contact casting or Aircast walkers boot
neuropathic ulcers develop in areas of injury or highest pressure
50% of diabetics get a foot ulcer
50% of pts with diabetes don’t know they have it
treated diabetic ulcers have a 50-70% recurrence risk in the next 5 years
Diabetic foot ulcers are often preventable with early recognition and intervention
diabetic foot ulcers are always neuropathic
Ischaemic diabetic ulcers have the best prognosis
Purely neuropathic ulcers have better prognosis than other 2 types
Most diabetic ulcers will eventually heal with good care
Only 1 third of diabetic foot ulcers will heal even with best care and those that do are slow, often more than 2 months
diabetics with foot ulcers have a higher mortality than those without
50% of lower limb amputations follow a diabetic foot ulcer
Diabetics have a 15-45x increased risk of lower limb amputation
How common is a contralateral amputation after a first lower limb amputation for diabetic complications?
50% risk of contralateral lower limb amputation within 5 years of first side amputation
What are the pathological factors in diabetic foot ulcers?
Neuropathy – motor, sensory and autonomic. Due to;
• Nitric oxide inhibition – increased ROS/superoxides
• Maillard reaction – results in advanced glycation end products
- Macrovascular disease
- Microvascular disease
- Thickening and loss of elasticity of capillary walls prevents vasodilatation
Inflammation & susceptibility to infection
What deformities can ocur in neuropathic feet?
‘cocked-up’ toe, claw toes and hammer toes - due to motor neuropathy
displaced plantar fat pads due to toe deformitys
halux valgus (bunions), hallux rigidus or equinus deformity of the ankle
Charcot or ‘rocker bottom’ foot and charcot ankle
What makes diabetic feet prone to infection and prolonged inflammation?
Loss of barrier when an ulcer forms allows entry of microbes
Bacteria grow in colonies surrounded by a biofilm
Diabetics have reduced chemotaxis and function
Reduced bactericidal and phagocytic capacity in the presence of hyperglycaemia
Sustained inflammation and delayed re-epithelialization contribute to slow healing
In diabetic foot disease callus indicates increased local pressure and portends an ulcer
Must examine both feet carefully with shoes and socks off
for callus neuropathy, pulses and deformity as well as ulcers
What are the International working group on the diabetic foot (IWGDF) risk categories and management recommendationd for diabetic foot disease?
Risk of ulcer and amputation goes up with category except 1 and 2 have zero risk of amputation
Should educate patient at all stages
0 - no sensory neuropathy
- Ulcer 2-6%, Amputation 0%
- revew annually
1 - Sensory neuropathy
- Ulcer 6-9%, Amputation 0%
- podiatry every 6 months + OTC shoes/ insoles
2 - Sensory neuropathy w/ deformity or PVD
- Ulcer 8-17%, Amputation 1-3%
- podiatry every 2-3 months + therapeutic shoes/ insoles
3 - Previous ulcer or amputation
- Ulcer 26-78%, Amputation 10-18%
- podiatry every 1-2 months + therapeutic shoes/ insoles
What are the 3 trongest risk factors fo diabetic ulcers?
Previous ulcer or amputation
presence of any 2 of these increases the risk by 32%
What are the most important things on examination of diabetic foot?
Callus or blister
Pulses (DP or PT)
How do you assess for neuropathy?
use sterile 10g monofilament on 10 areas – 4 insensate areas = positive test
128Hz tuning fork for vibratory perception
Test JPS in usual way
20-40% of pts develop diabetic sensorimotor polyneuropathy within 10 years of onset of diabetes
occurs sooner if glycaemic control is poor
presence of foot pulses reliably inicates absence of ischaemic foot disease
Palpable pulse indicates pressure of at least 80mmHg but is not a very sensitive indicator of the presence of PVD – 50% sensitivity and 73% specificity
Diabetics get calcium deposition in vessel wall (medial calcinosis) – pulse can be present but still poor perfusion
An ischaemic foot can appear pink and warm due to presence of shunts
Arterial Doppler (colour-coded duplex USS) and ABPI better to rule our arterial disease
Skin perfusion pressure can be measured by a vascular lab and may be helpful to diagnose critical ischaemia in diabetics
What a normal ABPI result?
systolic in ankle/foot divided by systolic in arm
Normal is 0.8 to 1.4
Toe-brachial pressure index is a better screening test than ABPI. Should be >55mmHg
Diabetes is most common cause of lower limb sensory neuropathy resulting in Charcot foot
What is Charcot foot?
A foot which is red, swollen and deformed often with dropped arch causing ‘rocker bottom’ appearance
Due to repetitive trauma to insensitive bones and joints of foot causing bones and joints to become dislocated
As process continues with partial healing fixed deformities develop in any or all parts of the foot and ankle causing the typical charcot appearance
Takes 6-9 months
What is the most likely diagnosis of a swollen, warm diabetic foot?
Osteomyelitis is the most likely diagnosis of swollen, warm foot with an ulcer;
Charcot foot most likely if swollen, warm diabetic foot and no ulcer
Which sites of diabetic ulcers heal best?
Forefoot wounds are more likely to heal than proximal ulcers
Heel ulcers are very poor to heal and have high amputation rates
Diagnostic overshadowing is a risk in an ulcerated diabetic foot
cna be skin cnacer including acral (amelanotic) melanoma
or other causes eg PG
classification/staging of ulcerated feet help to track progress
Meggit-Wagner classification – looks at wound depth and infection
IWGDF system classifies based on;
Perfusion, Extent (size), Depth, Infection & Sensation (PEDIS)
What parameters are assessed in the IWGDF system for diabetic foot ulcers?
What is the management of pt with diabetic foot/ulcer?
Hx including diabetic control, pain assessment and symptoms of vascular disease
- Check pulses
- Neuropathy test
- Callus and infection assessment
- Ulcer grading if ulcer present
- Assessment of skin around ulcer
- Assessment of bony abnormalities; bunions, hammer, claw, hallux rigidus, charcot
- Assess gait and footwear
Toe-brachial pressure index and/or arterial duplex
Xray and/or MRI if foot ulcer present or suspect charcot foot or osteomyelitis or both
FBC, ELFT, HbA1c, ESR & CRP (to look for comorbidities which may slow healing; anaemia, renal failure etc, albumin as marker of nutrition; inflammatory markers raised in osteomyelitis or other chronic disease; ESR >40 or CRP >20).
>50% of diabetic foot ulcers develop infection
every increase in HbA1c of 1% (0.01) over 0.07 results in 25% increased risk of peripheral artery disease
What are the definitions of;
Contamination – non replicating bacteria on wound surface (all wounds)
Colonization – replicating bacteria without a tissue response
Critical colonization – replicating bacteria in the superficial wound base with tissue damage
Infection – significant inflammation and tissue damage from replicating bacteria
swabs should be taken before a wound is cleaned and debrided
colonized to infected ulcers need antibiotics
nothing if colonized
topical antiseptics if critical colonization present E.g. povidone-iodine, honey, silver dressings, chlorhex
Antibiotics only if frnak infection - Start broad spectrum ABs first. At least 2 weeks for mild infection and 4 for severe. IV first if severe
What are the types of debridement of ucler?
sharp (surgical) - most often
Total contact cast is gold standard for redistributing plantar pressure in diabetic foot ulcers
redistribute pressure from forefoot to lower leg and heel
After healing, pts need therapeutic shoes which redistribute pressure to prevent recurrences
What are contraindications to Total contact casting?
heel ulcers (mainly need therapeutic shoes)
peripheral artery disease present
some compression can be used in mild arterial disease
Uncontrolled oedema delays healing of foot ulcers
Exudative wounds need absorbant dressings
foams, calcium alginates, hydrofibre
What kind of dressings good for dry wounds?
dressings which donate water – hydrogels
or which preserve water – acrylics, hydrocolloids, films
beware as all cal be occlusive and increase infection risk
If ulcer is not 50% healed by wk 4 with optimal care then unlikely to heal by wk 12
What are the advanced treatment options for diabetic ulcers which are not responding?
Growth factors e.g. recombinant human PDGF
Negative pressure wound therapy (vac dressing)
Hyperbaric oxygen therapy
Tissue-engineered skin equivalents - allograft, alloderm..
Autologous split skin graft
Surgical excision/ reconstruction
Surgical correction of foot deformities - rarly performed esp if active ulcer
amputation is last line
Negative presure VAC dressings are good for chronic non-healing wounds
Good for post surgical management of acute diabetic wounds
Not good for chronic non-healing wounds
How is Hyperbaric oxygen therapy delivered?
100% O2 delivered at >1 atm pressure
Sessions in a chamber last 45-120 mins
performed 1-2 times daily
4-5x per week up to 20-30 sessions in total
2/3 of AIDS pts have EMG evidence of peripheral nerve disease
80% of HIV +ve pts get xerosis possibly related to neuropathy of innervations of sweat glands
What is the classification of peripheral nerve injury?
- Injury causing myelin damage but axon still intact
- Loss of function but usually resolves in weeks-months
- Disruption of the axon but with intact perineurium
- Often from crush injury
- Causes sensory, motor and autonomic neuropathy
- Can recover over weeks-years
- Most severe form of nerve injury
- No possibility of full recovery
Carpal tunnel syndrome can cause skin changes
erythema of fingers, bullae, small foci of necrosis, nail dystrophy
What is ‘la main succulente’
French term for the appearance of the hands in Syringomyelia
skin over knuckles can become thick, swollen, cyanotic and keratotic due to chronic painless injury
Due to dissociated sensory loss with early involvement of the pain and temp fibres as they cross the cord in the anterior midline
tumours are the most common cause of syringomyelia
Type 1 Chiari malformation most common
(cerebellar tonsils extend below foramen magnum)
What is dysraphism?
How are they classified?
Raphe = a line of junction between 2 symmetrical embryological structures
Dysraphism is failure of complete fusion of these 2 structures
Occurs between week 2-6 of embryonic life when spinal cord is forming
classified as open or closed'
Open = Exposed to the environment e.g. spina bifida, myelomeningocele
Closed = Covered by intact skin
What skin features are associated with spinal dysraphism?
Pits or Dimples – lumbosacral dimples high risk whereas coccygeal dimple usually fine
Sinus ostia - opening of congenital dermal sinuses; pigment changes, erythema, skin tags, subcut masses
Giant congenital melanocytic naevus
Faun tail hypertrichosis
Vascular malformations or tumours – PWS, haemangioma
50% of cases have associated derm feature
get USS if concerned in child under 4 months or MRI if older
What are the features of Hereditary sensory and autonomic neuropathies?
5 types; 1-5
Genetic diseases; AD or AR
Present at birth except type 1 which presents later in childhood
Different combinations of loss of sensory, motor and autonomic motor neurones
Some get anhidrosis or excess sweating or pseudoainhum of fingers and spontaneous amputations
Often die in childhood some can survive w/ supportive cares
sympathetic nerve injury can prevent normal greying of hair
What are the types of Complex regional pain syndrome (CRPS) (Sudek's atrophy)?
CRPS type 1 (reflex sympathetic dystrophy) – no demonstrable nerve lesion, more common type
CRPS type 2 (causalgia) – nerve lesion on electrophysiology
Sudeck’s atrophy strictly refers to trophic changes in bone, muscle and skin
Complex regional pain syndrome is more common in women?
F:M = 4:1
Fractures are the most common cause of Complex regional pain syndrome
True - cause 50%
What skin condiitons can cause Complex regional pain syndrome?
Acrodermatitis continua of Hallopeau
Chronic venous ulcers
Minor surgery (nail or skin biopsy)
Idiopathic panniculitis (Weber-Christian)
How is the diagnosis of Complex regional pain syndrome made?
Diagnosis requires all 4 of;
1. Syndrome that develops after a noxious event
2. Spontaneous pain or allodynia/hyperalgesia not limited to the territory of a single nerve and disproportionate to the initiating stimulus
3. Past or present oedema, abnormal skin blood flow or sudomotor activity
4. Absence of other conditions that could account for pain or dysfunction
Complex regional pain syndrome made more commonly involves the legs than the arms
arms twice as common as legs
What are the derm features of Complex regional pain syndrome?
Skin is shiny, atrophic and dry (‘trophic’ change due to altered innervations)
Sudomotor changes (hyper then hypo hidrosis)
Erythema and warmth
Hyper or hypo trichosis
Hyper or hypo hidrosis
Beau’s lines, nail notching, leukonychia, onychodystrophy
capsaicin and EMLA creams are helpful in Complex regional pain syndrome?
need systemic neuropathic pain agents and other drugs from pain specialist as well as procedural interventions and psychotherapy
What is Cutaneous dysaesthesia?
chronic skin symptoms without any objective findings
What is burning scalp syndrome? How is it treated?
Pts often complain of itching or burning or stinging pain of the scalp
Triggered or exacerbated by psychological or physical stress
Often middle aged or elderly women
Often anxiety, depression or stressful life event
No objective findings - need full work up, scrapings, biopsies, APT etc
Low dose SSRI – better response in pain than itch types
What is burning feet syndrome? How is it treated?
Idiopathic or assoc w/ diabetic neuropathy
Can be AD trait
Can be found in those w/ minor foot deformities like high arches
Loss of small fibre sensory nerves
Mainly cholinergic defects – unlike other autonomic neuropathies which are adrenergic
Burning sensation of feet exacerbated by heat or by cold
May have dry skin, eyes or mouth
May have vasomotor symptoms of peripheral coldness, burning or flushing, HTN or impotence
- Dopaminergic agents – levadopa, cabergoline
- Pramipexole, ropinirole, rotigotine (non-ergot dopaminergic agents) have less risk of heart or lung fibrosis
2nd line agents
- Opioids – endone, codeine, methadone
- BZs – diazepam, clonazepam
o Iron supplements only if ferritin low (
What is burning mouth syndrome? How is it treated?
Burning mucosal pain with no lesions
Usually bilateral on anterior 2/3 tongue, palate and lower lip
buccal mucosa and floor of mouth are rarely involved
7x more common women, esp mid age or older
Type 1) 35% - fine on waking, symptoms increase over day
Type 2) 55% - constant burning day and night
Type 3) 10% - interspersed affected days and days of remission with no cause found
Precipitating factors – deficiency of iron, zinc, folate, Vit B12; T2DM; hypothyroid; menopause, drugs
Assessment – look carefully for lesions esp SCC, trauma from ill-fitting dentures, candida, LP, xerostomia, contact dermatitis from dental work, glossitis, geographic tongue
Must review ALL meds – stop any that can cause xerostomia (anticholinergics etc)
Screen for depression/anxiety
Treat cause if found
Consider referral to dentist, psych etc if any indication
Worth a course of antifungals even if culture negative – nilstat
If primary (no cause found) try; amitryptaline, doxepin, benzos, gabapentin
Topical local anaesthetic
Topical steroid + CBT and α-lipoic acid
What is 'Tic douloureux'
Recurrent paroxysms of sharp pain lasting secs-mins in a territory of one of the sensory divisions of CN.V
No skin changes, sensory and motor nerve function is normal
Trigeminal neuralgia is more common on the right side than the left
Trigeminal neuralgia attacks can be triggered by touching face, eating, talking, brushing teeth
Up to 18% of Trigeminal neuralgia pts have MS but without demonstrable demyelination of trigeminal nerve
How is Trigeminal neuralgia managed?
Fullexam of skin and asessment of sensory component of nerve and local motor nerves
MRI indicated if suspicious of another cause of symptoms
Exclusion of reversible cause needed to make diagnosis
Carbamazepine most effective oral agent – helps in 70-90%
Phenytoin – IV for acute crisis
Surgery if refractory – microvascular decompression, stereotactic radiosurgery (gamma radiation) has had some good results