Neurology Flashcards
1
Q
Differential diagnosis of Headaches
A
Migraine, Tension headaches, Cluster headaches, Temporal Arteritis/ GCA, Medication Overuse headaches, Meningitis, Encephalitis, Subarachnoid haemorrhage, Sinusitis
2
Q
If the patient presents with ‘Thunderclap headaches’, what is the most worrisome differential diagnosis
A
Subarachnoid haemorrhage
3
Q
Facial nerve palsy: Defintion
A
Isolated dysfunction of the facial nerve. This typically presents with a unilateral facial weakness
4
Q
CN7 pathway & branches
A
The facial nerve exits the brainstem at the cerebellopontine angle. On its journey to the face it passes through the temporal bone and parotid gland.
Branches: Temporal, Zygomatic, Buccal, Marginal mandibular, Cervical
5
Q
CN7 Function
A
There are three functions of the facial nerve: motor, sensory and parasympathetic.
Motor: Supplies the muscles of facial expression, the stapedius in the inner ear and the posterior digastric, stylohyoid and platysma muscles in the neck.
Sensory: carries taste from the anterior 2/3 of the tongue.
Parasympathetic: it provides the parasympathetic supply to the submandibular and sublingual salivary glands and the lacrimal gland (stimulating tear production).
6
Q
Facial nerve palsy: UMN vs LMN lesion
Why is it important to distinguish between them?
A
UMN: forehead- sparing (each side of forehead is innervated by both sides of then brain)
LMN: non-forehead sparing (each side of forehead only supplied by LMN from one side of brain)
7
Q
LMN facial palsy: presentation
A
On affected side:
No-movement of forehead
Drooping eyelids, exposing eye
loss of nasolabial folds
8
Q
UMN facial nerve palsy: causes & 2 main conditions/syndrome
A
UMN lesion: strokes, space-occupying lesion (tumour/ bleed)
Bilateral UMN lesions (rare): MND & pseudobulbar palsies
Conditions:Bell’s palsy & Ramsey Hunt syndrome
9
Q
Bell’s palsy:cause, diagnosis, prognosis & management
A
Cause: idiopathic
Prognosis: Most recover completely but 20-30% have permanent facial weakness or paralysis
Diagnosis: Unilateral facial weakness with no identifiable cause
Management: 10 day Prednisolone 25mg BD within 72 hrs. Anti-virals (eg. acyclovir/ valacyclovir) not indicated. Lubricating eyedrops to prevent eye from drying out. . If they develop pain in the eye they need an ophthalmology review for exposure keratopathy. Tape can be used to keep the eye closed at night.
10
Q
Ramsey Hunt syndrome: cause, presentation & management
A
Cause: (cephalic/varicella) Herpes Zoster Virus
Presentation: unilateral facial weakness with painful, tender vascular rash around ear, ear canal and can extend down anterior 2/3 of tongue and hard palate. auditory dysfunction. taste perceptionn and lacrimation may also be affected
Management: Prednisolone & Acyclovir/valacyclovir within 72 hours. Lubricating eyedrops also required
11
Q
Bilateral LMN facial nerve palsy: common causes
A
Lyme disease & GBS
12
Q
Most common causes of unilateral vs bilateral facial nerve palsy
A
Unilateral: Herpes zoster (Ramsey-Hunt syndrome)
Bilateral: Lyme disease (bacteria: Borrelia burgdoferi) & GBS
13
Q
A 40-year-old man comes to the emergency department because of bilateral facial weakness during the past 3 days. He also reports a change in
taste
sensation. One month ago, he had
flu-like
symptoms after returning from a climbing trip in New York. Physical examination shows flattening of the
skin
of his forehead. Motor examination shows difficulty with facial movements bilaterally, including smiling and raising his eyebrows. The remainder of the examination shows no abnormalities. Which of the following is the most likely diagnosis?
A
Major takeaway
Bilateral facial nerve palsy is often associated with untreated Lyme disease. Unilateral palsy is often idiopathic and may be associated with herpes zoster
infection.
Main explanation
This patient’s symptoms of facial weakness, loss of wrinkling of the forehead, and change in taste sensation are consistent with a bilateral facial nerve (cranial nerve VII) palsy. Bilateral facial nerve palsy is rare compared to unilateral involvement and is most commonly associated with Lyme disease and Guillain-Barré syndrome. Patients typically have a sudden onset of symptoms, which can be concerning for a stroke; however, most patients will make a full recovery, with signs of recovery seen within 3 weeks. Lyme disease is a tick-borne illness caused by the bacteria Borrelia burgdorferi. The disease is endemic to the northeastern United States and is often seen in hikers or others who spend time outdoors. Patients may report an initial flu-like syndrome that often goes ignored. The classic sign is erythema migrans, a “bulls-eye”rash with central clearing. If untreated, cardiac and neurologic manifestations, including bilateral facial nerve palsy, may occur.
14
Q
Causes of LMN CN7 palsy
A
Infection: Otitis media, Malignant otitis externa, HIV, Lyme’s disease
Systemic disease: Diabetes, Sarcoidosis, Leukaemia, Multiple sclerosis, Guillain–Barré syndrome
Tumours: Acoustic neuroma, Parotid tumours, Cholesteatomas
Trauma: Direct nerve trauma, Damage during surgery, Base of skull fractures
15
Q
Dementia: Definition
A
Acquired, progressive cognitive impairment involving one/more cognitive functions.
16
Q
Dementia: examples of cognitive and non-cognitive effects
A
Cognitive functions: language, comprehension, judgement and planning & other executive functions
Non-cognitive effects: personality, mood, emotional control, behaviour & psychosis
17
Q
Dementia: Types of functional impairment
A
Agnosia: ability to recognise objects, persons, sounds, shapes or smells
Anosognosia: lack of ability to perceive the reality of one’s own deterioration
Apraxia: inability to perform learned (familiar) movements on command, even though the command is understand and there is willingness to perform task
Apathy: lack of feeling and interest
18
Q
Dementia: Risk factors
A
Key: advancing age
Non-modifiable
- Age
- Genetics
- PMHx: Hearing loss & depression
Modifiable
- Cognitive reserve: leaving education early, less job complexity & social isolation
- Increased inflammation: central obesity and infection
19
Q
Dementia: Early stage
A
Often overlooked as gradual onset.
Common symptoms
- forgetfulness
- losing track of time
- becoming loss in familiar places
Can be attributed to normal aging
20
Q
Dementia: Middle stage
A
Presentation becomes clearing
- forgetful of recent events and people’s names
- becoming confused while at home
- having increased difficulty with communication
- needing help with personal care
- experiencing behaviour changes, including wandering and repeated questioning
21
Q
Dementia: late stage
A
Near total dependence and inactivity. Memory disturbances are serious and physical signs and symptoms becoming more obvious
- becoming unaware of time and space
- having difficulty recognising relatives and friends
- having an increasing need for assisted self-care
- having difficulty walking
- experiencing behaviour changes that may escalate and include aggression
22
Q
Dementia: Types and distribution
A
Alzheimers: 50-70%
Vascular Dementia: 20-30%
DLB: 10-25%
FTD: 10-15%
23
Q
Dementia: Differential histology findings
A
Alzheimers:
- extracellular accumulation of senile plaque (amyloid peptides): vessel wall deposits correlate with injury
- Intraneuronal neurofibrillary tangles (NFTs): Better predictor of cognitive decline
- Neuronal loss
Vascular dementia:
- cerebral artery atherosclerosis
- carted artery/heart embolisation
- vasculitis
- small white matter infarcts (Brain MRI) (absent cortical atrophy)
DLB:
- Alpha-syneiclein protein aggregation in neurons (particularly cortex, substantial nigra) -> Lewy bodies -> apoptosis
FTD:
- Associated with specific cellular inclusions: tau proteins (Pick disease) & TDP-43
24
Q
Dementia: Inx
A
Bloods: FBC, U&E, glucose, LFTs, calcium, ESR & CRP, Folate & B12, TFTs, syphilis serology
Imaging: Chest X-ray, CT/MRI
25
Dementia: Causes (reversible & non-reversible)
Degenerative: Alzheimers, DLB, FTD, Huntington and Parkinson, NPH, Primary progressive aphasia
Vascular: cerebral haemorrhage, cerebral infarct/ atherosclerosis
Metabolic: uraemia, hepatic failure & paraneoplastic syndromes
Endocrine: Hypothyroidism & hypocalcaemia
Toxic: alcohol, o
Infection: syphilis, CJD, HIV, Whipple's disease
Deficiency: Alcohol excess/withdrawal, folate & B12 deficiency, thiamine
26
Dementia: Key differential characteristics of Ddx
Vascular: 'step-wise' decline. CVD risk factors & history
FTD: 40-65 yr old. memory loss develops after behavioural changes/ personality disturbances, language and movement
DLB: Parkinsonism (bradykinesia, tremors and rigidity) developed <1 year after cognitive decline, REM sleep disorder, visual hallucination (early stage)
Alzheimers: advanced age, FHx - gradual memory loss (episodic then romantic)
27
FTD: 2 most common types
1. Frontal variant: affects behaviour and personality
| 2. Primary progressive aphasia: language
28
Alzheimers: Treatment
- Acetylecholinesterase inhibitor: donepezil (mild-moderate), rivastigmine (if main symptom: hallucination)
- NMDA receptor antagonist (memantine): advanced neuroprotective and DMARD
- Vitamine E supplements
29
DLB: Management
Goal: Alleviate symptoms
- Acetylcholinesterase inhibitors: doneprazil & rivastigmine (visual hallucinations)
- Dopamine analoge (motor symptoms)
30
FTD: Treatment
Goal: Alleviate symptoms
- Anti-depressants (severe behavioural symptoms)
- Atypical antipsychotic drugs (significant SE)
- Atypical antipsychotics eg. haloperidol and risperidone.
31
Vascular dementia: treatment
Vascular risk factor control: anti-HTN, anti-DM, statins, anti-platelet agents
Acetylcholinesterase inhibitors/ memantine
32
Delirium: Definition & subtypes
Clinical syndorme characterised by disturbed consciousness, cognitive function or perception. Acute onset with fluctuation course
Subtypes: Hyperactive (75%), Hypoactive (25%)
33
Delirium: Causes
Surgery
Systemic infection: sepsis, UTI, malaria, pneumonia, IV line/catheter
Intracranial infection/ head injury
Drugs/ drug withdrawal: opiates, levodopa, sedatives, recreational
Alcohol withdrawal (2-5s post-admission; increased LFTs, increased MCV; Hx of EToH abuse
Metabolic: uremia, liver failure, Na+ or glucose, low Hb, malnutrition (beriberi)
Hypoxia: respiratory or cardiac failure
Vascular: stroke, MI
Nutritional: thiamine, nicotinic acid or B12 deficiency
34
Delirium: DDx
Dementia
Psychiatric: schizophrenia, anxiety, epilepsy (non-convulsive status epilepticus = under diagnosed)
35
Delirium: Inx
Goal: Look for cause
Bloods: FBC, ESR/CRP, U&E, Glucose, ABG, septic screen (urine dipstick, CXR, blood cultures)
Consider: ECG, malaria films, Lumbar Punture, EEG & CT
36
Delirium: Management
Identify & treat cause
Other aims:
- Re-orientate patient; explain where they are and who you are at each encounter
- encourage family visits
- monitor fluid balance and encourage oral intake. Beware for constiption
- Mobilise and encourage physical activity
- Practice sleep hygiene: restrict daytime napping, minimise might-time disturbance
- Avoid/ remove catheters, IV cannulae, monitor leads and other devices
37
Delirium vs Dementia
Acute vs Chronic (trends & Hx)
Inattention, Disorganised thinking & Distractibility -> Delirium
38
Brain metastasis: Prevalence and most common primary sites
Affects 40% of patients with cancer
Site: lung, breast, colorectal & melanoma
39
Brain metastasis: Prognosis
Poor prognosis
Median survival: 1-2 months
Better prognosis with single lesion, best cancer
40
Brain metastasis: Presentation
```
Space occupying lesion: headache (often worse in morning, when coughing/ bending),
Focal neurological signs,
Ataxia,
Fits,
N&V,
Pallioedema
```
41
Brain metastasis: Management
Imaging: Urgent head MRI/CT
Disease stage and performance status
Reduce cerebral oedema: Dexamethasone 16mg/24hr
Stereotatic radiotherapy
42
Chronic Fatigue Syndrome: Diagnosis
Chronic fatigue ≥ 24 hrs
+ 4 symptoms: myalgia, polyarthralgia, unrefreshing sleep, fatigue after exertion after 24 hrs. decreased memory, persistent sore throat or cervical lymphadenopathy
43
CFS: Management
CBT & graded exercise
Pharmacological management (same as fibromyalgia), shown ineffective for CFS:
- Amitriptyline - relieve pain and improve sleep
- Pregabalin - if amitriptyline ineffective
- Duloxetine or SSRI: co-morbid depression and anxiety
Steriods/ NSAIDs not recommended.. no inflammatory process
44
CFS: Yellow flags
Psychosocial risk factors to developing chronic pain
Belief that exercise will worsen pain
Problems attaining benefits
Social withdrawal
Sickness behaviour eg. extended rest
Overprotective family or lack of support
Emotional problems eg. depression, anxiety / stress
Inappropriate expectations of treatment eg. low active participation in treatment
45
ME/CFS: Cause
Research suspect an infection may trigger ME/CFS: EBV (glandular fever), Ross Rive virus, Coxiella brunetti.
HHV-6, rubella, Candida albicans, bornavirus. mycoplasma and HIV
Bacterial infection: pneumonia
Immune system changes
Hormone imbalanceStress affect body chemistry: HPA axis regulates immune response, digestion, energy usage and mood. Lower cortisol can lead to inflammation and immune suppression (levels normal for CFS patients therefore not diagnostic marker)
Possible genetic link
46
Encephalitis: Definition
Acute inflammation of brain parenchyma due to direct invasion/pathogen-initiated immune response
Often assoc. with meningitis
47
Encephalitis: Route of infection
Peripheral nerve conduits to brain parenchyma for viral infection - rabies, HSV
haematogenous spread -> transfer of infection from distant sites
48
Encephalitis: Causes
Viral: HSV-1 (most common) & HSV-2
EBV, HIV, VZV (varicella-zoster virus), measles, mumps, rabies. influenza
Non-viral: any bacterial meningitis, TB, malaria, syphillis, listeria, Lyme disease, legionella, leptospirosis, aspergillosis
49
Encephalitis: Risk factors
Immunosuppression,
Travel to low-income nations,
Exposure to disease vectors in endemic areas
50
Encephalitis: Complications
Seizures,
SIADH
Increased ICP
Coma
51
Encephalitis: Presentation
General red flags: fever, chills & malaise
Meningeal involvement (meningism): nuchal rigidity, headache & photosensitivity
Parenchymal involvement: focal neurological sings, seizures, altered mental state.
History of travel or animal btes
52
Encephalitis: Inx
Bloods: blood & CSF cultures, glucose, toxoplasma IgM titre, malaria film
Contrast CT: Focal bilateral temporal lobe involvement suggestive of HSV encephalitis. meningeal enhancement suggests meningoencephalitis. Do before LP.
MRI alternative if allergic to contrast
Lumbar puncture: moderately increased CSF protein and lymphocyte and decreased glucose. Send CSF for viral Per including HSV
EEG: urgent EEG showing diffuse abnormalities may help diagnosis of encephalitis but doesn't indicate cause.
53
Encephalitis: Treatment
Viral encephalitis:
- HSV: acyclovir
- CMV: ganciclovir/foscarnet
Bacterial encephalitis
- Targeted antibodies
54
Encephalitis: Prognosis
Mortality in untreated encephalitis is 70%
55
Cerebral abscess: pathology
localised focal necrosis of brain tissue with inflammation, usually caused by bacterial infection
rare (de novo within brain, primary infection typically arises elsewhere, spreads to brain)
56
Cerebral abscess: Presentation
Classic Triad (20% of cases)
- Fever, progressive worsening focal neurology, headache
- Increased ICP while supine -> worse headache early morning, at night/ increased ICP stimulates medullary centre, area postrema -> morning vomiting
Mental status change, seizures, nausea & vomiting, papilloedema
57
Cerebral abscess: Inx
CT/MRI (eg. ring-enhancing lesion)
Bloods: Increased CRP, ESR & wCC.
Special: Abscess aspirate - biopsy, LP (increased WCC = increased protein concentration, normal glucose content)
58
Cerebral abscess: Treatment
Urgent neurosurgical referral: Drainage & removal of foreign material
Medication
- Targeted Abx therapy: penetration through abscess wall poor, typically accompanies surgical management
- Hyperbaric O2 therapy: reduce ICP, bacteriostatic, enhances oxidative immune function
- Corticosteroid in complicated cases with pituitary insufficiency
59
Diabetic Neuropathy: Defintion
Peripheral nerve damage secondary to DM.
Depending on affected nerves, diabetic neuropathy symptoms: pain & numbness in legs, feet and hands. It can also cause problems with digestive system, urinary tract, blood vessels and heart.
60
Diabetic Peripheral neuropathy: Presentation
Distribution: Glove & stocking (most common) distribution. May be patchy
Absent ankle jerks
```
Neuropathic deformity (Charcot foot): pes cavus, clawed toes, loss of transverse arch, rocker-bottom sole
Caused by loss of sensation -> increased mechanical stress on pressure points and repeated joint injury. Swelling, instability & deformity.
```
Painful neuropathy: numbness, burning or shooting pain, tingling and/or paraesthesia of the hands and/or feet typically in a stocking and glove distribution, often at night. Over time it can progress to persistent neuropathic pain
61
Diabetic Automatic Neuropathy: presentation
Can affect multiple systems
Postural hypotension
Gastroparesis (delayed gastric emptying). Unexplained diarrhoea
Inadequate bladder emptying,
Sexual disfunction eg. erectile dysfunction
Sweating abnormalities & impaired awareness of hypoglycaemia
62
Diabetic Foot: Prevention and services
Refer early; podiatry, imaging, vascular surgery
Amputations common (135/week): warn patients & educate to monitor their feet weekly for signs of change eg. using mirror to monitor soles
63
Diabetic foot: Vascular ischemia vs peripheral neuropathy
Ischaemia: Critical toes +/- 'punched out' ulcers, absent pulses
Neuropathy: Injury/ infection over pressure points eg. metatarsal heads.
64
Diabetic foot: Ischaemia presentation & Management
Absent foot pulses
Critical toes; gangrene
Management
- education
- regular chiropody: remove callus, as haemorrhage and tissue necrosis may occur below -> ulceration
- treat fungal infections:
- surgery eg. endovascular angioplasty balloon, stents & subintimal recanalisation.
65
Diabetic neuropathy: Foot ulceration
Typically painless, punched our ulcer in area of thick callus +/- superadded infection. Causes cellulitis, abscess +/- osteomyelitis
Asses degree of:
1. Neuropathy (clinically)
2. Ischaemia (critical toes, absent foot pulse)
3. Bony deformity eg. Charcot foot (clinically & x-ray)
4. Infection (swabs, blood culture, x-ray for osteomyelitis, problem ulcer to reveal depth)
Management: regular chiropody. bed rest & therapeutic shoes
- Charcot's joints: bed rest/ crutches/total contact cast until oedema and local warmth reduce and bony repair complete ( ≥8 weeks). Bisphosphonates may help
- Cellulitis: admit for IV Abx. Common organisms: staphs, streps, anaerobes.
66
Diabetic neuropathy: Charcot's foot symptoms
Swelling
Warmth
Change in foot colour
Change in foot shape: loss of transverse arch, rocker bottom sole.
67
Diabetic neuropathy: Absolutely indications for surgery in ulcerated foot
Abscess/ deep infections
Spreading anaerobic infection
Ischemic Limb: gangrene/rest pain
Suppurative arthritis
68
Diabetic neuropathy: Four main types
Symmetrical sensory polyneuropathy: glove & stocking distribution.
- tingling & numbness. pain. worsens at night
- Rx: paracetamol -> Tricycline (amitriptyline) -> Duloxatine -> gabapentin -> opiate
Autonomic neuropathy
- Postural hypotension
- Vagal neuropathy: loss of respiratory sinus arrhythmia
- Gastroparesis
- Unexplained diarrhoea
- Gustatory sweating
- Sexual dysfunction eg. erectile dysfunction
- Urine retention
```
Mononeuritis multiplex (eg. CN3 & CN6)
- If sudden & severe -> Rx: immunosuppressants eg. Prednisolone, IV Ig, ciclosporin
```
Amyotrophy
- Muscle wasting of quadriceps muscle +/- pelvifemoral muscles
- Imaging: electrophysiology.
69
Epilepsy: Defintion
Recurrent seizures of unknown causes. Spontaneous, intermittent and abnormal brain waves.
Convulsions = motor signs of electrical discharges
70
Epilepsy: elements (prior and post) of seizures
Prodrome: lasting hours/days prior to seizure.
- change in mood or behaviour
Aura: can be focal seizure of temporal lobe
- strange feeling of gut, deja vu, strange smells, flashing lights
Post-ictal
- headache, confusion, and myalgai
- Todd's paralysis: temporary weakness after focal seizure in motor cortex
- dysphasia following focal seizure of temporal lobe
71
Epilepsy: Causes of epileptic seizure
2/3 cases idiopathic
... increased excitation: long-lasting/ fast activation of NMDA receptors via glutamate
... decreased inhibition: genetic mutations -> dysfunction GABA receptors
Disorders: brain injury, brain abscess, brain tumours, eclampsia, encephalitis, Angelman syndrome
CVD: ischaemia stroke, intracranial bleeding, perinatal hypoxia, ischaemia
Systemic disorder: Uremic encephalopathy, hepatic encephalopathy, eletrolyte imbalance (Na, Mg & Ca), hypoglycaemia, thiamine deficiency, Vitamin B12 deficiency
72
Epilepsy: Causes of provoked seizures
| SICKDRIFT3R
Substrate: glucose, O2
Isoniazid
Cations: Na, Mg & Ca
Kids: pregnancy, eclampsia
Drugs: aminophylline, bupivacaine, bupropion, butyrophenones.
Recreational: amphetamines, cocaine, methylphenidate, psilocybin, psilocin (present in psychedelic mushrooms)
Rum: alcohol +/- withdrawal
Illness (chronic): Tuberous sclerosis, sarcoidosis, SLE, Ig targeting VGKC
Fever: febrile seizures
Trauma
3 anti: histamine, depressants, convulsants
Rat poison
73
Epilepsy: Inx
Bedside:
- EEG
- Neuro exam: assess behaviour, motor abilities, mental functions
- > underlying seizure cause & type
- Glucose
- Urine sample
Bloods: FBC (WCC - inflammation/ vasculitis), U&E, LFTs, renal function
Imaging: MRI/CT scans
- detect structural abnormalities
74
Epilepsy: Focal vs Generalised. Subtypes.
Focal: initially stems from localised brain region; limited to one hemisphere
- Focal aware: patient awake & alert. No impaired consciousness
- Focal impaired awareness: unilaterally affects large area of one hemisphere. Individual loses awareness; responsiveness; does not remember seizure. Most commonly in temporal lobe -> post-ictal features
- 2dary generalised
Generalised: engages both cerebral hemispheres. No localising features referable to single hemisphere.
- Absence seizure
- Febrile seizure
- Tonic
74
Epilepsy: Focal vs Generalised. Subtypes.
Focal: initially stems from localised brain region; limited to one hemisphere
- Focal aware: patient awake & alert. No impaired consciousness
- Focal impaired awareness: unilaterally affects large area of one hemisphere. Individual loses awareness; responsiveness; does not remember seizure. Most commonly in temporal lobe -> post-ictal features
- 2dary generalised
Generalised: engages both cerebral hemispheres. No localising features referable to single hemisphere.
- Absence seizure
- Febrile seizure
- Tonic: rigid stage. falls backwards
- Clonic: convulsion stage
- Tonic-Clonic: Post-ictal stage included
- Myoclonic: sudden, brief, involuntary muscle jerks lasting 1-2s.
- Infantile spasm
- Atonic: sudden muscle relaxation; forward falling
75
Epilepsy: Localising features of focal seizures
Temporal lobe
- Automatisms: complex motor phenomena with impaired awareness
Primitive oral (lip smacking, chewing, swallowing)
Complex actions
- Dysphasia
- Deja vu/ jamais vu (everything seems strangely unfamiliar)
- Emotional disturbance eg. sudden terror, panic anger or elation and derealisation
- Hallucinations of small, taste or sound
- Delusional behaviour
- Bizarre association
Frontal lobe
- Motor features: posturing or peddling movements of legs
- Jacksonian march
- Motor arrest
- Subtle behavioural disturbances
- Dysphasia or speech arrest
- Post-ictal Todd's palsy
Parietal lobe
- Sensory disturbances: tingling, numbness, pain (rare)
- Motor symptoms: die to spread to pre-central gyrus
Occipital lobe
- Visual phenomena: spots, lines & falshes
76
Epilepsy: Management for each syndrome
AEDs: only commended after epilepsy diagnosis of ≥2 seizures. Choice depends on subtype, lifestyle, co-morbidities and patient's preferences
Treat cause: if reversible, known cause
Focal: 1st line: carbamazepine or lamotrigine. 2nd: levetiracetam, oxcarbazepine or sodium valproate
Absence seizures: 1st line: Sodium valporate or ethosuximide (children). 2nd: lamotrigine
Myoclonic: 1st: sodium valporate. 2nd: levetiracetam or topiramate (increased SE). Avoid carbamazepine and oxcabazepine - may worsen
General tonic-clonic: 1st Sodium valporate or lamotrigine. 2nd: carbamazepine. clobazam, levetiracetam or topiramate
Other interventions: Psychological therapies eg relaxation, CBT.
77
Essential tremor: pathology
Most common movement disorder: involuntary, rhythmic, shaking
Usual sites: hands, fingers. Sometimes head, vocal cords
```
Action tremor (occurs during muscle effort)
- postural/ intention tremor
```
78
Essential tremor: causes
Mainly idiopathic
| Familial: autosomal dominant inheritance pattern
79
Essential tremor: Risk factors
- Meat consumption: heterocyclic amines (eg. germane, harmaline) exposure
- Associated with dystonia (cervical, spasmodic, cranial dystonia, writer's cramp), parkinsonism
80
Essential tremor: Presentation
Rhythmic, symmetrical tremor
- hands, head, vocal cords, neck, face, leg, tongue, trunk
High frequency tremor (4-12Hz) exacerbated by muscle contraction
Inability to perform precise tasks
Intention tremor
- Intensifies upon touching nose with finger
Postural tremor
- during outstretched arms
Walking difficulties
Decreased tremor with alcohol intake
81
Essential tremor: Diagnosis
Physical examination
- Fine postural, active tremor in hands, head/voice
- Asymmetric/symmetric: cogwheel rigidity, resting tremor, dystonia (esp. head)
Other diagnostic:
- postural/ action tremor of hands/head; duration ≥ three years
- alleviation with alcohol intake
82
Essential tremor: Treatment
Medications: If disabling, symptomatic treatment
- Beta-blockers: propranolol
- Anti-epileptics: Primidone. 2nd line: Gabapentin and topiramate
- Benzodiazepine: alprazolam or clonazepam
- Botulinum toxin (hand tremor not responsiveness to medication)
Lifestyle Modification
- avoid caffeine, nicotine etc
- get enough sleep
83
Essential Tremor vs Parkinson's tremor
Laterally: Symmetrical vs Asymmetrical
Kinetics: Movement/posture vs Resting
Speed: High frequency vs Slow
Involvement: Arms, legs, voice, neck, face & tongue vs Hands, legs & chin
84
Meniere's Disease: pathology
Increased pressure in endolymphatic system of inner ear.
| Causing vertigo, progressive hearing loss
85
Meniere's Disease: Causes
Exact cause unknown: likely abnormal fluid, ion homeostasis in inner ear (endolymphatic hydrops)
Possibly due to endolymphatic sac/ duct blockage, viral infection, vestibular aqueduct hypoplasia, vascular constriction
86
Meniere's Disease: Risk factors
Children - congenital inner-ear malformation
FHx: 10% familiar
87
Meniere's Disease: Presentation
Recurrent vertigo lasting >20min
Fluctuating (or permanent) sensorineural hearing loss
Tinnitus
(with sense of fullness +/- falling to one side)
Associated symptoms: fatigue, nausea & vomitting
Less common: drop attack
88
Meniere's Disease: Diagnosis
Diagnostic criteria:
- 2+ unprovoked vertigo episodes (each lasting >20 mins)
- Audio-metrically confirmed sensorineural hearing loss in affected ear on at least one occasion before/during/after vertigo attack
- Tinnitus/fullness feeling in ear
89
Meniere's Disease: Management
Pharmacological:
- Antihistamines - cinnarizine, buccal prochlorperazine if severe
- Antiemetics,
- Anticholinergics
Surgery: if symptoms don't improve
- surgical decompression of endolymphatic sac
Other interventions
- Sodium restrictoin
- Diuretics
90
Meningitis: Defintion
inflammation of meninges coning CSF. Mainly caused by bacterial/ viral infection
91
Meningitis: Meningococcal septicaemia
Meningococcus bacterial infection of bloodstream
Causes 'non-blanching rash' (maculopapular): caused by DIC (disseminated intravascular coagulopathy) and subcutaneous hemmorhages
92
Meningitis: Bacterial causes
Most common in children & adults
- Neisseria meningitidis (meningococcus)
- diplococci
- Streptococcus pneumonia (pneumococcus)
Neonates: Group B Streptococcus (GBS)
- usually contracted during birth as present in mother's vaginal canal
93
Meningtis: Presentation
Insidious onset with fever, malaise, N&V
Later meningism: headache, vomiting, nuchal/back rigidity, photophobia, altered consciousness
Kernig’s test:
lying the patient on their back, flexing one hip and knee to 90 degrees and then slowly straightening the knee whilst keeping the hip flexed at 90 degrees. This creates a slight stretch in the meninges and where there is meningitis will produce spinal pain or resistance to this movement.
Brudzinski’s test:
lying the patient flat on their back and gently using your hands to lift their head and neck off the bed and flex their chin to their chest. A positive test is when this causes the patient to involuntarily flex their hips and knees.
94
Meningitis: Complication
Complications up to 20% of patients
- sensorineural hearing loss
- imparted vestibular funciton
- epilepsy
- diffused brain injury
95
Meningococcaemia: Presentation
Mild: Fever, maculopapular rash w/out shock
```
High-grade: pyrexia and septic shock within 6-12hrs due to rapidly escalating endotoxin levels
- Circulatory failure
- coagulopathy with skin haemorrhage
- thrombosis of extremities/adrenals
- AKI
- ARDS
+/- meningism
```
96
Meningococcaemia: Complications
```
Amputation,
Skin necrosis,
Pericarditis,
Arthritis,
Ocular infection,
Pneumonia (esp. serotype Y & W),
Permanent adrenal insufficiency
```
97
Meningitis: Management (Inx & Management)
Start Abx immediately if suspected.
Intra & extracellular diplococci on microscopy: CSF/blood/skin lesion
PCR: CSF/ blood/ skin lesion
Treatment: urgent Abx treatment
- If non-blanching rash in 1st care: Benzylpenicillin
- 1st line: ceftriaxone
- Other bactericidal: cefotaxime, chloramphenicol, meropenem
Prevention:
- routine infant vaccination against capsular group C in UK
- capsular group B vaccination
Prophylaxis of contacts:
- ciprofloxacin/ ceftriaxone (single dose)
- rifampicin 600mg BD or 48h
98
Viral meningitis: Causes & presentation compared to bacterial
Most common:
- Herpes simplex virus (HSV),
- Enterovirus and varicella zoster virus (VZV).
A sample of the CSF from the lumbar puncture should be sent for viral PCR testing.
Viral meningitis tends to be milder than bacterial and often only requires supportive treatment.
99
Viral meningitis: Treatment
Aciclovir can be used to treat suspected or confirmed HSV meningitis
100
Meningitis: Lumbar puncture results (bacterial vs viral)
The spinal cord ends at the L1-L2 vertebral level so the needle is usually inserted into the L3-L4 intervertebral space.
```
Appearance: Cloudy vs Clear
Protein: High vs Mildly raised or normal
Glucose: Low vs normal
White Cell Count: High (neutrophils) vs High (lymphocytes)
Culture: Bacteria vs Negative
```
101
Meningitis: Complications
Sensorineural hearing loss,
Cognitive impairment & learning disability
Seizures & Epilepsy
Memory loss
Focal neurological deficit: limb weakness/ spasticity
102
MND: Defnition
Progressive, ultimately fatal condition where motor neurones stop function. Characterised by selective loss of neurones in motor cortex, cranial nerve nuclei and anterior horn cells
No effect on sensory neurones and patients should not experience any sensory symptoms.
103
MND: Differentiation from MS, polyneuropathies and myasthenia
MS & polyneuropathy:MND has no sensory loss or sphincter disturbance
Myasthenia: MND has no effect on eye movements
104
MND: 4 clinical patterns
ALS/ amyotrophic lateral sclerosis (80%)
- loss of motor neurones in motor cortex and anterior horn of cord
- combined UMN & LMN signs
- worse prognosis if: bulbar onset, increased age & decreased FVC
Progressive bulbar palsy (10-12%)
- only affects CN 9-12
Progressive vascular atrophy (<10%)
- LMN only: anterior horn cell lesion
- affects distal muscle group before proximal
- prognosis: better than ALS
Primary lateral sclerosis (rare)
- Loss of Betz cells in motor cortex: mainly UMN signs
- marked spastic leg weakness and pseudobulbar palsy
- no cognitive decline
105
MND: Presentation
Think MND in >40 yrs (median UK age 60M) with stumbling spastic gait, foot drop +/- proximal myopathy, weak grip and shoulder abduction or aspiration pneumonia
UMN signs: spasticity, rigidity, brisk reflex and upping plantar response
LMN: muscle wasting, reduced tone, fasciculation (tongue, abdomen, back & thigh) and reduced reflexes
Bulbar signs: dysarthria
106
MND: Diagnosis
Based on clinical presentation and exclusion
Brain/ cord MRI to exclude structural cause
LP: exclude inflammatory cause
Neurophysiology: detect subclinical denervation and help exclude mimicking motor neuropathy
107
MND: Prognosis
Poor: <3 years post onset for 50% of patients
108
MND: Management
No effective treatments for halting/ reversing disease... MDT approach
Riluzole (Inhibit glutamate release and NMDA receptor antagonist)
- slow progressive of disease
- extend survival by a few months
Symptomatic treatment:
- Excess saliva: advice on positioning oral care and suctioning. Try anti-muscarinic (eg. propantheline) or Botulinim may help
- Dysphagia: blend food, gastrostomy is an option
- Spasticity: exercise, orthotics
- Communication difficulty: provide alternative communication method
- Palliative care
109
Multiple sclerosis Definiton
Inflammatory plaques of demyelination in the CNS disseminated in space and time in multiple sites. Neurodegenerative condition involving demyelination of neurones and poor healing leading to axonal loss.
This is caused by an inflammatory process involving the activation of immune cells against the myelin.
110
MS: Classic Demographic
Typically presents in:
- young adults (under 50 years). Median 30hrs
- more common in women: 3:1
Symptoms tend to improve in pregnancy and in the postpartum period.
111
MS: Neurones affected
Schwann cells in:
| CNS: oligodendrocytes
112
MS: Causes
Causes unknown... hypothesis: vitamin D & role of infection
Genetics: multiple genes
Infection: EBV (epstein barr virus)
Low Vitamin D
Smoking Obesity
113
MS: Common Presentation
Usually mono-symptomatic:
- 20% present with unilateral optic neuitis: pain on eye movement and decreased rapid central vision
Common: involvement if corticospinal tract & bladder
Symptoms worsen with heat
114
MS: Other presentation
Focal weakness
- Bells palsy
- Horners syndrome
- Limb paralysis
- Incontinence
- erectile dysfunciton & anorgasmia
Focal sensory symptoms
- Trigeminal neuralgia
- Numbness
- Paraesthesia (pins and needles)
- Lhermitte’s sign: electric shock sensation that travels down the spine and into the limbs when flexing the neck. indicates disease in the cervical spinal cord in the dorsal column. It is caused by stretching the demyelinated dorsal column.
Ataxia
- Sensory ataxia: result of loss of the proprioceptive sense, which is the ability to sense the position of the joint (e.g. is the joint flexed or extended).
- This results in a positive Romberg’s test and can cause pseudoathetosis.
- Cerebellar ataxia is the result of problems with the cerebellum coordinating movement. This suggestions cerebellar lesions.
115
MS: Disease patterns
Highly variable between individuals
Clinically isolated syndrome: first ep. of demyelnation & neurological presentation. May not develop MS
Relapsing-remitting: most common pattern at initial diagnosis
- Active: new symptoms/ lesions are appearing on MRI
- Not active: no new symptoms or MRI lesions are developing
- Worsening: overall worsening of disability over time
- Not worsening: there is no worsening of disability over time
Secondary Progressive: RR developing into progressive worsening of symptoms with incomplete remissions.
Symptoms become more permanent.
- Active: new symptoms/ lesions are appearing on MRI
- Not active: no new symptoms/ MRI lesions
- Progressing: overall worsening of disease over time (regardless of relapses)
- Not progressing: there is no worsening of disease over time
Primary Progressive: worsening of disease and neurological symptoms from the point of diagnosis without initial relapses and remissions.
Similar classification as secondary progressive
116
MS: Diagnosis
Neurologist based: clinical picture & symptoms suggesting lesions that change location over time
Symptoms progressive over a period of 1 year to diagnose primary progressive MS. Other causes for the symptoms need to be excluded.
Investigations:
- MRI scans: demonstrate typical lesions
- Lumbar puncture can detect “oligoclonal bands” in CSF
117
Optic Neuritis: Presentation
Unilateral reduced vision developing over hours to days
Key features are:
- Central scotoma. This is an enlarged blind spot.
- Pain on eye movement
- Impaired colour vision
- Relative afferent pupillary defect
118
Optic neuritis: defintion
Inflammation of the optic nerve
119
Optic Neuritis: Causes
```
Multiple sclerosis is the main cause,
Sarcoidosis,
Systemic lupus erythematosus (SLE)
Diabetes,
Syphilis,
Measles,
Mumps,
Lyme disease
```
120
Optic Neuritis: management
Urgent referral to ophthalmologist after acute vision loss
Treatment: Steroids (Prednisone) 2-6 weeks
121
Optic neuritis: Complciation
50% of patient develop MS over next 15 years.
| MRI changes can predict likelihoo
122
MS: Management
MDT: neurologist, specialist nurse, physiotherapist, occupational health other others
Education: Condition and treatment
Disease-modifying drugs:
- Mild RR MS: Dimethyl fumarate, Alemtuzumab (Monoclonal Antib. acts against T cells) and natalizumab (acts against VLA-4 receptors that allow immune cells to cross BBB),
Azathioprine is not recommended due to its SE profile.
- Treating relapses: Methylprednisolone, eg 0.5–1g/24h IV/PO for 3–5d shortens acute relapses; use sparingly
Symptom control:
- Spasticity: baclofen or gabapentin.
2nd line: Tizanidine or dantrolene
if these fail consider benzodiazepines.
- Tremor: botulinum toxin type A injections
- Urgency/frequency: if post-micturition residual urine >100mL, teach intermittent self-catheterization; if <100mL, try tolterodine.
- Fatigue: amantadine, CBT, and exercise may help.
123
MG: Defintion
Myasthenia graves is an autoimmune condition that causes muscle weakness that gets progressively worse with activity and improves with rest.
124
MG: Antibody involved
85%: Ab against nicotinic acetylcholine receptors (AChR)
Location: post-synaptic NMJ
15%: Ab against muscle-specific kinase (MuSK) & low-density lipoprotein receptor related protein 4 (LRP4).
- fewer proteins to make AChR receptor
Both B&T cells indicated
125
MG: Presentation
Muscle weakness worsen with exertion and improves with rest. Symptoms minimal in morning and worse at end of day.
Mostly affect proximal muscles and small muscles of the head and neck:
- Extraocular muscle: diplopia
- Eyelid weakness: ptosis
- Weakness in facial movements
- Difficulty with swallowing
- Fatigue in the jaw when chewing
- Slurred speech
- Progressive weakness with repetitive movements
126
MG: Exacerbating factors
```
Pregnancy,
hypokalaemia,
infection,
change of climate,
emotion,
exercise,
Drugs: gentamicin, opiates, tetracycline, quinine & beta-blockers, over treatment
```
127
MG: Associations
Autoimmune diseases (RA and SLE)
if <50 yrs: more in women & thyme hyperplasia
> 50 yrs: more in men & thyme atrophy tunic tumour
128
MG: Examination (elicit fatigue)
- Repeated blinking will exacerbate ptosis
- Prolonged upward gazing will exacerbate diplopia on further eye movement testing
- Repeated abduction of one arm 20 times will result in unilateral weakness when comparing both sides
Check for a thymectomy scar.
Test the forced vital capacity (FVC).
129
MG: diagnosis
Ab testing:
- ACh-R antibodies (85% of patients)
- MuSK antibodies (10% of patients)
- LRP4 antibodies (less than 5%)
Imaging: CT/ MRI of thymus gland for thymoma.
Edrophonium test: helpful where doubt is present.
130
MG: Treatment
- Reversible acetylcholinesterase inhibitors (usually pyridostigmine or neostigmine)
- Immunosuppression (e.g. prednisolone or azathioprine)
Surgery: Thymectomy can improve symptoms even in patients without a thymoma
Monoclonal antibodies
- Rituximab: Monoclonal antibody targeting B cells and reduces the production of antibodies.
- Eculizumab is a monoclonal antibody that targets complement protein C5. This could potentially prevent the complement activation and destruction of acetylcholine receptors. (not NICE recommended)
131
MG: Myasthenic crisis
Severe complication & can be life threatening.
It causes an acute worsening of symptoms, often triggered by another illness such as a RTI leading to respiratory failure as a result of weakness in the muscle of respiration.
132
Myasthenic crisis: Management
Ventilation: non-invasive ventilation with BiPAP or full intubation and ventilation.
Medical treatment: immunomodulatory therapies (IV Ig) and plasma exchange
133
Parkinson's: Pathology
Degeneration of dopaminergic neurones in substantial nigra -> dopamine depletion from basal ganglia
Protein (alpha-synuclein) accumulation in neuron. Build up of Lewy bodies in neurones accompanied by death of astrocytes
134
Parkinson's: Extrapyramidal triad
1. Tremor: resting tremor; pin-rolling
2. Hypertonia: rigidity + tremor = 'cogwheel' rigidity
3. Bradykinesia: slow to initiate movement
135
Parkinson's: Causes
Usually idiopathic,
Genetic loci: PINK1 mutation, Parkin, alpha synuclein gene,
Toxicity in recreational drugs MPPP (rare)
136
Parkinson's: Risk factors
Mean onset: 80-85 yrs
PMHx: previous head injury, pesticide exposure.
FHx
Protective factors: nicotine & caffeine
137
Parkinson's: Presentation
Triad: tremor, bradykinesia, Hypertonia
Non-motor symptoms:
Autonomic dysfunction (postural hypotension, constipation, urinary frequency/urgency, dribbling of saliva),
Sleep disturbance,
Reduced sense of smell (common 1st symptom)
Neuropsychiatric: common & debilitating
Depression
Dementia
Psychosis
138
Parkinson's: Diagnosis
Clinical diagnosis
- Triad presentation & dopaminergic medication response
- Exclude: cerebellar disease & FTD/ DLB
Postmortem autopsy
Imaging: MRI to exclude other structural defects
139
Parkinson's: Treatment
| SALAD
Symptom management
Selegiline
Anticholinergics: (improves neurochem. imbalance)
- trihexyphenidyl, benzhexol, orphenadrine
L-Dopa + peripheral decarboxylase inhibitor:
- carbidopa, benserazide
Amantidine (anti-viral - known NMDA agonist)
Dopamine postsynaptic receptor agonist:
- bromocriptine, lisuride, pergolide
Surgery: Deep brain stimulation (DBS)
- Increase motor output of basal ganglia -> decrease motor symptoms
- Severe disease
Other intervention
- Education, support
- Physical therapy
140
Parkinson's: Complication
Freezing phenomenon: progressive hypokinesiai & bradykinesia -> akinetic pauses In movement
Falls: 2nd to postural instability, poor movement amplitude
Dystonia: abnormal tone across joint
Dementia: common after prolonged, primarily motor disease
( > 1 yr post memory deficit onset)
141
Peripheral Neuropathy: Specific causes (DAVID)
```
Diabetes Mellitus (most common)
Alcoholism
Vitamin B12 deficiency
Infection: GBS, EBV, leprosy, sarcoidosis
Drugs eg. isoniazid, amiodarone, pyridoxine, nitrofurantoin
```
142
Peripheral Neuropathy: 6 main mechanism
1. Demyelination – e.g. GBS, post-diphtheric neuropathy, hereditary sensory-motor neuropathies
– usually occurs as a result of schwann cell damage.
2. Axonal degeneration
– usually occurs in toxic neuropathies
– conduction speed remains normal, and the axon tends to dies of peripherally first, then more proximally. Surviving axons often strive to re-innervate affected areas
3. Wallerian degeneration: fibre degeneration when the fibre is cut or crushed.
- Both the axon & myelin sheath will degenerate over several weeks after the incident.
4. Compression: e.g. carpal tunnel syndrome
– there is local demyelination at the site of compression. Occurs when the compression is not as severe as in wallerian degeneration.
5. Infarction: polyarteritis nodosa, Churg-Strauss syndrome, diabetes
– there will also be wallerian degeneration distal to the infarct.
6. Infiltration – e.g. leprosy, malignancy, inflammation, sarcoidosis
143
Peripheral neuropathy: presentation
Altered sensation, pain, weakness or autonomic symptoms
Symptoms normally start distally -> Proximal
Classic picture of advanced polyneuropathy:
- distal wasting & weakness
- absent tendon reflexes
- glove & stocking sensory loss
143
Peripheral neuropathy: presentation
Altered sensation, pain, weakness or autonomic symptoms
Symptoms normally start distally -> Proximal
Classic picture of advanced polyneuropathy:
- distal wasting & weakness
- absent tendon reflexes
- glove & stocking sensory loss
144
Peripheral neuropathy: Distribution
Symmetrical, generalised, multifocal or focal
Symmetrical generalised polyneuropathy: distal-to-proximal gradient in "stocking-glove" pattern
Mononeuropathy Multiplex: almost simultaneously dysfunction of several peripheral nerves. Frequently painful and cause weakness.
Focal neuropathy (mononeuropathy): Trauma & entrapment of peripheral nerves.
145
Peripheral neuropathy: Most freq. seen entrapment neuropathies (mononeuropathy)
• Median nerve across the wrist (carpal tunnel syndrome)
• Ulnar nerve across the elbow (tardy ulnar palsy)
• Radial nerve at the spiral groove (Saturday night palsy)
• Peroneal nerve at the fibular head (peroneal nerve palsy)
• Distal branches of the tibial nerve at the ankle (tarsal tunnel
syndrome)
146
Peripheral Neuropathy: Inx
Bloods:
- Urine: glucose & protein. Heavy metal screen (Hg, Pb, Zn & As)
- Haematology: FBC, ESR, vitamin B12 & folate
- Biochemistry: Fasting BGC, Renal function, LFT, TSH
Neurophysiological tests: Assessment of distal & proximal nerve stimulation
Biochemistry: Serum protein electrophoresis, serum ACE
Immunology: Anti-nuclear factor, Anti-extractable nuclear antigen antibodies (anti-Ro, anti-La), anti-neutrophil cytoplasmic antigen ab)
Imaging: CXR - screen for asymptomatic LC
147
Sensory Neuropathy: Cause and presentation
Cause: DM, CKD, leprosy
Presentation: numbness, paraesthesia, difficulty handing small objects
- Glove & stocking distribution
- Signs of trauma or joint deformation may indicate sensory loss
Diabetic & Alcoholic neuropathies can be painful
148
Motor Neuropathy: Cause and Presentation
Case: GBS, lead poisoning. Charcot-Marie-Tooth syndrome
Presentation:
- Often progressive (may be rapid)
- Weak/ clumsy hand
- Difficulty in walking (falls/ stumbling)
- Difficulty breathing (decreased FVC)
Signs
- LMN: muscle wasting and weakness in distal muscles of hands & feet (foot/ wrist drop). Reflexes reduced/ absent
149
Peripheral neuropathy: Pharmalogical Treatment
Treating Cause
- GBS & CIDP: IV Ig & corticoid steroids (pred. for CIPD only)
- Vasculitis: steroids/ immunosuppressants (Azathioprine, methotrexate, cyclophosphamide)
```
Neuropathic pain (Tricyclic): amitriptyline, duloxetine, gabapentin or pregabalin
- Use: bring, dysesthetic pains with peripheral neuro.
```
Anticonvulsants: carbamazepine, phenytoin & lamotrigine.
- Treat lancinating pain with trigeminal neuralgia
150
Peripheral Neuropathy: Support Intervention
Involve physiotherapy and occupational therapy
| Foot care and shoe choice - aim to reduce trauma
151
Radiculopathy: Definition
Conduction block in axons of spinal nerve or its roots, with impact on motor axons causing weakness and on sensory axons causing paraesthesia &/or anaesthesia
NOT SPINAL CORD (cord compression) therefore more localised effect
152
Radiculopathy: Causes of nerve compression
Intervertebral disc prolaspe: rupture of annulus fibrosis and sequestration of disc material
Degenerative diseases of spine: lead to neuroforaminal or spinal canal stenosis
- Cervical spine = most mobile segment of the spine and degenerative change is a normal part of ageing process
- 80% of the population over 55 years old have degenerative changes between C5/6 and C6/7
Fracture: trauma/ pathological
Malignancy: most commonly metastatic (lung, breast, prostate and kidney)
Infection: extradural abscess, osteomyelitis (Pott's disease) or herpes zoster
153
Radiculopathy: Presentation
Sensory features: paraesthesia and numbness
Motor features: weakness
Radicular pain often present
- Typically described as a burning, deep, strap-like, or narrow pain. It is not uncommon for radicular pain to be intermittent.
Identify red flags: faecal incontinence, urinary retention, saddle anaesthesia
154
Radiculopathy: Presentation vs Location of impingement
C5 (C4/5 disc)
- Motor/ sensory: weak deltoid & supraspinus. Decreased supinator jerks; numb elbow
- Pain: neck/ shoulder that radiates down from front of arm to elbow
C6 (C5/6 disc)
- M/S: weak biceps & branchioradialis; decreased bicep jerks, numb thumb & index finger
- Pain: shoulder radiating down arm below elbow
C7 (C6/7 disc)
- M/S: weak triceps & finger extension; decreased tricep jerks; numb middle finger
- Pain: upper arm and dorsal forearm
C8 (C7/T1)
- M/S: weak finger flexors & small muscle of hand; numb 5th & ring
- Pain: upper arm and medial forearm
155
Radiculopathy: Definitive LT Mangement
Definitive long-term management depends on the underlying cause. Only condition requiring emergency surgical is CES.
Most IV disc prolapses managed non-operatively
Indications for surgical treatment
- Unremitting pain despite good conservative management
- Progressive weakness
- New/progressive myelopathy (Spinal cord compression)
156
Radiolopathy: Symptomatic Mangement
Analgesia using WHO analgesic ladder in the first instance.
However neuropathic pain meds. are frequently used.
- 1st line: Amitriptyline. Alternative: pregabalin & gabapentin
- SE: Muscle spasms managed with diazapam / baclofen.
Physiotherapy remains an important part of management in this patient group.
157
Spinal Cord compression: Definition
Malignant cord compression: radiological evidence of indentation of the thecal sac secondary to cancer.
158
Anatomy: Vertebral level of end of spinal cord
L1/L2
159
Spinal cord compression: Cancers associated with SCC 2nd to metastatic disease
Lung, Breast, kidney, prostate and thyroid cancer
160
Spinal cord compression: Causes
Malignant compression (Primary and Secondary)
Other causes:
- Trauma
- Intervertebral disc prolaspe
- Haematoma
- Epidural abscess (2ndary to osteomyelitis/ discitis)
- Cervical spondylitis myelopathy
161
Spinal Cord Compression: Presentation
Requires high degree of suspicion: presentation can be subtle
- pain, motor and sensory symptoms & bladder and bowel involvement
Cord compression: Back pain, paralysis, hyperreflexia, positive babinski's
Cauda equina: Back pain, radiculopathy, reduced anal tone, saddle anaesthesia, paralysis, hyporeflexia, hypotonia.
162
Spinal Cord Compression: Diagnosis
Imaging: MRI for suspected malignant cord compression
- determination of extent of disease
- accurate identification of site of compression
Other possible modalities:
- Myelography
- Computed tomography
- Bone scan
- Plain radiographs
Bloods: FBC & coagulation screen, inflammation markers, B12, syphillisserp;pgu, u&E, LFT, PSa, serum electrophoresis
163
Spinal Cord Compression: Management
Acute cord compression & CES = surgical emergencies
General measures:
- Analgesia
- Refractory pain: Refer to pain team
- VTE prophylaxis
- TED stockings na prophylactic LMWH
Urgent Dexamethasone - malignancy (& receive oedema)
- Radio/chemo therapy dependant on tumour type +/- decompressive laminectomy
Epidural abscess -> surgically decompressed and Abx
164
Stroke: Prevalence
Common medical emergency.
- Total strokes: ~ 110,000/ yr
- 11% mortality rate after 1st stroke
- 1/2 survivors suffer with permanent disability
```
Ischaemic stroke (85%): occlusion of vessels
Haemorrhage (15%): bleeding
```
165
Stroke: Definition
Cinical syndrome characterised by sudden onset of rapidly developing focal or global neurological disturbance
- Lasting > 24 hours/ death.
166
Stroke: Causes
Ischaemia
- Thrombosis: local blockage by atherosclerosis
- Precipitating: CVD risks or small vessel disease (vasculitis, sickle cell)
- Emboli: AF or carotid artery disease, endocarditis, dialted cardiomyopathies, rheumatic valve disease
- Dissection (rare): spontaneous/ 2dary to trauma
Haemorrhage:
- HTN (most common)
- Non-traumatic ICH: vascular malformation (AV malformation/ fistula), brain tumour, vasculitis/ bleeding disorders. Aneurysm rupture, anti-coagulant/ thrombolysis
- Trauma
167
Haemorrhagic stroke: Presentation
Global features:
- Headache
- Altered mental state
- Nausea & Vomiting
- Hypertension
- Seizures
Focal neurological deficits (dependent on location of bleed)
168
Cerebral Ischaemic stroke: Location & Differential presentation
Anterior:
- Unilateral weakness and/or sensory deficit: face (leg>arm)
- Homonymous hemianopia
- Higher cerebral dysfunction: dysphasia, visuospatial dysfunction (e.g. neglect, agnosia). impaired judgement and incontinency
Middle:
- Unilateral contralateral weakness: face & (arms>leg)
- Slurred speech (dysphagia)
- hemispatial neglect
- homonymous hemianopsia
- deviation of eye to left side
Posterior: vertebrobasilar arterial system
- Dizziness
- Diplopia
- Dysarthria & Dysphagia
- Ataxia
- Visual Field defects
- Brainstem syndromes: often seen with crossed signs*
169
Posterior stroke syndromes: 2 main types
Brainstem syndrome:
Wallenberg syndorme: Posterior inferior cerebellar artery syndrome (PICA)
- dizziness, nystagmus, speech, swallowing difficulties
- Ipsilateral: facial sensory loss, Horner's sign & ataxia
- Contralateral: loss of pain, temperature sensation in limbs
Locked in syndrome: Basilar artery
- dizziness, gait, vision disorders, dysarthria, dysphagia
- plegia of head, body muscles, except eye; only blinking and vertical movement possible
170
Wallenberg syndrome/ Lateral medullary syndorme: Features
- Nystagmus
- Vertigo
- Ipsilateral Horner’s syndrome
- Ipsilateral facial sensory loss
- Dysarthria & dysphagia
- Diplopia
- Contralateral pain and temperature loss
171
Lacunar infarcts: Locations and 5 syndromes associated
Location: Basal ganglia, internal capsule, thalamus & pons
5 syndrome: ataxic hemiparesis, pure motor, pure sensory, sensorimotor and dysartheria/ clumsy hand
Cognition/ consciousness intact except thalamus infant
172
Stroke: Diagnosis
Urgent referral: stroke unit
Imaging Head CT/MRI:
- Urgent < 1hr: if haemorrhagic stroke suspected
- Less urgent < 24hrs
NIHSS score & clinical history
Bedside: observations, blood glucose, ECG (AF)
Bloods: FBC, U&Es, Bone profile, LFT, ESR, coagulation, lipid profile, HbA1c
Imaging: CT head +/- CT angiography +/- MRI head
Special: Echocardiography, carotid dopplers, 24 hour tape, young stroke screen
173
Stroke: DDx (stroke mimics)
Toxic/metabolic: hypoglycaemia, drug & alcohol consumption
Neurological: seizure, migraine, Bell’s palsy
Space occupying lesion: tumour, haematoma
Infection: meningitis/encephalitis, systemic infection with ‘decompensation’ of old stroke
Syncope: extremely uncommon presentation of TIA, many other causes
Non-organic: functional neurological disorders (FND)
174
Stroke: NIHSS score
Out of 42: predictive score of clinical outcome in stroke
- Imp. in considering thrombolysis in clinical outcome
Score <4: good clinical outcome
Score >22 (high): significant proportion affected by ischaemia
- higher risk of haemorrhage with thrombolysis (contra.)
175
Stroke: Management
Establish blood flow in ischaemic penumbra
- Thrombolytic enzymes: rtPA, alteplase given wtihin 4.5 hrs
- Antiplatelet: aspirin +/- clopidogrel
Hypertension treatment
-IV Labetalol/ nicardipine
cerebral oedema managment
- Antipyretic: if temperature > 39C
- IV insulin: hyperglycaemia
