Neuro Flashcards
Bell’s Palsy - Definition & Presentations
Bell’s palsy is an acute unilateral peripheral facial nerve palsy in patients for whom physical examination and history are otherwise unremarkable
It consists of deficits affecting all facial zones equally that fully evolve within 72 hours
Diagnosis of exclusion
Presentations:
- Single episode
- Unilateral
- Involvement of all nerve branches
- Pain
- Keratoconjunctivitis sicca (dry eye - dysfunction of lacrimal glands)
- Synkinesis (involuntary and abnormal synchronous movement of a facial region concomitant with reflex or voluntary movement in another facial region and may occur only as a late sequela of Bell’s palsy)
-Fever, general malaise, myalgia, arthralgia, headache, or rash (erythema migrans or other) suggests an alternative diagnosis, such as Lyme disease, autoimmune disorder, or granulomatous disease.
Bell’s Palsy - Aetiology & Risk Factors
Strong evidence points to reactivation of herpes simplex virus type 1 (HSV-1) within the geniculate ganglion as the underlying cause of Bell’s palsy
Correlation between facial palsy and coronavirus disease 2019 (COVID-19) has been demonstrated, but not confirmed - the same with the COVID-19 vaccine
Risk Factors:
- Intranasal influenza vaccination (vaccine no longer in use)
- Pregnancy (3x more likely)
Bell’s Palsy - Epidemiology
Bell’s palsy is the most common aetiology of unilateral facial palsy among those aged 2 years and older. It is most prevalent in people aged 15-45 years.
The reported incidence is 23-32 cases per 100,000 per year
Equally distributed between both sexes
No substantial evidence that seasons, geographical locations, racial or ethnicity affects developing Bell’s palsy
The incidence of Bell’s palsy is higher during pregnancy -> Pregnancy-associated Bell’s palsy is associated with a lower chance of recovery.
Bell’s Palsy - Differentials
1) Herpes Zoster Oticus (Ramsay Hunt Syndrome)
-> Otalgia (ear pain), sensorineural hearing loss (caused by lesion), vertigo, vesicles on skin of external canal
2) Lyme disease
-> Target-like bite/rash
-> Hx of being in woods/ places with Ticks
-> Frontal headache, fever, malaise, fatigue
3) Benign facial nerve tumour
-> Waxing and waning or slowly progressive facial palsy
-> May demonstrate uneven distribution of weakness across facial zones, with elements of synkinesis and fasciculations
4) Malignant facial nerve tumour
-> Insidious and slowly progressive onset of facial palsy
-> Palpable parotid mass
-> Hx of skin cancer of ipsilateral face, especially squamous cell carcinoma
5) Blunt force trauma to face/temporal bone
-> Hx of recent head trauma with immediate or delayed-onset facial palsy
Bell’s Palsy - Investigations
1st Order:
- Based on examination and Hx, diagnosis of exclusion
- Serology for Borrelia Burgdorferi (to exclude Lyme Disease)
- Needle Electromyography -> should see absence of voluntary motor unit potentials
- Electroneuronography -> >90% decrease in the amplitude of compound muscle action potential (CMAP) on the affected compared with the healthy side is an indication for confirmatory needle electromyography
Bell’s Palsy - Management
1st Line:
- Oral Corticosteroid w/in 72 hours of symptom onset
-> Improves long-term outcomes and shortens time to recovery
-> Be careful w/ children, poorly controlled diabetes, immunodeficiency, poorly controlled hypotension and prior hx of psychosis
-> Exclude Lyme disease as steroids may worsen long-term outcomes in these patients
-> prednisolone: 60 mg orally once daily for 5 days, then decrease by 10mg every day after
- Eye protection due to Keratoconjunctivitis sicca
-> Glasses + Artificial tears
-> use lubricant on eyes and tape eyelids shut during sleep
Bell’s Palsy - Prognosis & Complications
The extent of facial palsy following complete evolution of Bell’s palsy (i.e., within 72 hours of onset) is the parameter most predictive of ultimate recovery outcome. Of those who present with incomplete flaccid paralysis on clinical examination, 94% will fully recover, compared with 61% of those who present with complete flaccid paralysis
Poor prognostic factors:
- Advanced age
- Diabetes mellitus
- Taste disturbance on presentation
- Electroneuronography (ENoG) revealing a >95% difference between sides within 14 days of symptom onset
Complications:
- Keratoconjunctivitis sicca -> Can cause dry eyes, leading to corneal ulcers, which can lead to blindness
- Ectropion (sagging eyelid) -> This may occur during the acute flaccid phase of Bell’s palsy and rarely persists
- Contracture & Synkinesis -> Shortening of muscles/tendons/skin, Involuntary movement accompanying a voluntary movement
-> The likelihood is 16% to 29% in the absence of treatment
-> he suspected mechanism is increased neural irritability and aberrant regeneration of motor axons - Gustatory Hyperlacrimation -> tearing excessively in response to salivary stimuli
-> long-term complication of Bell’s palsy due to aberrant regeneration of pre-ganglionic parasympathetic fibres carried within the facial nerve that supply the lacrimal gland and mucosal glands of the nasal cavity and palate
-> Botulinum toxin to the lacrimal gland has demonstrated effectiveness in the long-term management of this complication
Benign paroxysmal positional vertigo (BPPV) - Definition & Presentations
A peripheral vestibular disorder
Caused by crystals from the otolith organ getting into the semi-circular canals and irritating the hair cells in the canals responsible for detecting head movements.
Causes sudden, short-lived episodes of vertigo elicited by specific head movements
Often self-limiting, but can become chronic and relapsing with considerable effects on a patient’s quality of life
Benign paroxysmal positional vertigo (BPPV) - Aetiology & Risk Factors
Approximately 50% to 70% of BPPV occurs without a known cause and is referred to as primary (or idiopathic) BPPV
The remainder is termed secondary BPPV and is associated with a range of underlying conditions, including:
- Head trauma
- Labyrinthitis
- Vestibular neuronitis
- Meniere’s disease (endolymphatic hydrops)
- Migraines
- Ischaemic processes
- Iatrogenic causes
Risk Factors:
- Increasing age
- Female sex
- Head trauma
- Migraines
- Inner ear surgery
- Vestibular neuronitis
- Labyrinthitis
Benign paroxysmal positional vertigo (BPPV) - Epidemiology
Primary BPPV peak incidence between 50 and 70 years of age, but can occur in any age group
Migraine and head trauma are more common in younger patients with secondary BPPV compared with older patients with secondary disease
Female sex more likely to be affected
High rate of unrecognised BPPV
Benign paroxysmal positional vertigo (BPPV) - Differentials
1) Meniere’s disease
-> There is associated hearing loss, tinnitus, and aural fullness that is often exacerbated during an episode of vertigo.
-> Recurrent episodes of vertigo last for minutes to hours and are not provoked by positional changes
2) Vestibular neuronitis
-> Often a single episode of persistent vertigo lasting for days. The vertigo can be exacerbated by any positional change, unlike the specific head movements that induce BPPV attacks.
-> May be preceded by a non-specific viral infection
3) Labyrinthitis
-> Often a single episode of persistent vertigo lasting for days. The vertigo can be exacerbated by any positional change, unlike the specific head movements that induce BPPV attacks.
-> May be preceded by a non-specific viral infection. Hearing loss is present in viral labyrinthitis
4) Perilymphatic fistula
-> Accompanied by hearing loss, tinnitus, and aural fullness (blocked/pressure in ear)
5) Central disorders (i.e. migraines, ischaemic processes, MS…)
->Headaches, visual symptoms, other sensory abnormalities such as paraesthesia or deficits, and motor abnormalities all suggest a central aetiology
-> Vertigo not precipitated by specific head movements
-> Central disorders can mimic BPPV attacks; however, symptoms tend to have a more gradual onset and to be less severe and less transient
Benign paroxysmal positional vertigo (BPPV) - Investigations
1st Order investigations:
1) Dix-Hallpike manoeuvre -> Used to diagnose posterior canal BPPV ( can be used to diagnose rare anterior canal varient)
-> Lay patient down, with head tilted 30 degrees back and 45 degrees to the side. Watch their eyes for Nystagmus (movement of the eyes), indicating vertigo.
-> Should be reversable when sitting, and fatigable w/ repeat testing
-> Left ear BPPV has a clockwise torsional nystagmus response, while right ear BPPV has an anti-clockwise response
2) Supine Lateral Head Turns -> Used to diagnose lateral (horizontal) canal BPPV
-> The clinician places the patient in a supine position and, ideally, flexes the neck 30° from horizontal to bring the lateral canals into the vertical plane of gravity. However, it is sufficient and more usual to simply lay the patient flat on their back
-> The head is then rotated to one side, left for 1-2 minutes, and then rotated to the opposite side
-> A positive test is noted when the patient experiences vertigo with nystagmus
Can also do:
- Audiogram -> If hearing loss (Primary BPPV not associated w/ hearing loss)
- Brain MRI -> exclude Central causes
Benign paroxysmal positional vertigo (BPPV) - Management
Acute Management:
- Reassurance that BPPV is non-life threatening and usually responds well to treatment
- Teach/ refer to specialist for head manoeuvres
If Manoeuvres fail:
- Surgery, if all else fails and it is still debilitating. All other diagnoses must first be excluded
Benign paroxysmal positional vertigo (BPPV) - Prognosis & Complications
One third of patients remit at 3 weeks and the majority of patients at 6 months from onset
However recurrences are common even after successful treatment with repositioning manoeuvres, so further treatments may be required
Poor Prognosis:
Meniere’s disease (endolymphatic hydrops), central nervous system diseases, migraine headaches, and post-traumatic BPPV have all been associated with a greater risk of recurrence
Complications:
- During treatment the patient can become extremely nauseous, vomiting is not uncommon
- Accidents related to constant vertigo in everyday life
-> Falls in older patients
- Sometimes during treatment the manoeuvres can cause the crystals to transfer to another canal instead of to the otolith organ
Myalgic encephalomyelitis - Definition & Presentations
Also called Chronic fatigue syndrome, however it is more than just fatigue.
Characterised by:
- post-exertional malaise (PEM)/exertional exhaustion –> Most characteristic feature
- a sudden or gradual onset of persistent disabling fatigue
- unrefreshing sleep
- cognitive and autonomic dysfunction
- myalgia
- arthralgia
- headaches
- sore throat
- tender lymph nodes (without palpable lymphadenopathy)
Symptoms last at least 6 months
Fatigue is not related to other medical or psychiatric conditions, and symptoms do not improve with sleep or rest
