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Neurology

1) Functional disorders like non-epileptic attack disorder
Functional disorders are those which have no pathological cause but still
present with symptoms (IBS as an example, or fibromyalgia)
...

They can be thought of as interference with signals from the brain from the
emotional centres
...

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•

•
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Lesions below L1/2 are LOWER
motor neuron lesions as they are
after the spinal cord ends, even if they
are in the spinal column

Useful drugs:
•
•

Haloperidol – antipsycotic used in
schizophrenia and delirium
...
Also used in
MS
MAOB inhibitors – inhibit the
catabolism of dopamine in the
brain

Sensory – these can be positive or negative symptoms
...
This can be very difficult for patients
...

Concentration, memory and fatigue – patients may find they have
trouble concentrating or remembering things
...

Movement symptoms – people may have difficulty moving
...


Chronic fatigue syndrome (CFS) – it occurs most commonly in women between 20 and 50
...
Poor concentration, impaired memory, Alteration in
sleep and muscular pain are all common
...
Treatment includes communication and
explanation of the disease, stopping drugs (e
...
caffeine), cognitive behaviour therapy and antidepressants for mood disorders
Without treatment less that 10% recover within 1 year
...

Fibromyalgia (chronic widespread pain) – this overlaps with CFS but has more diffuse muscle and joint pain
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Functional brain scans suggest that patients perceive greater pain and support the idea of abnormal sensory processing
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Tricyclics have been
shown to have the greatest effect on sleep, fatigue and pain
...
The main sites are the head, lower back,
abdomen, genetalia and neck
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Brain scans suggest the brain responds poorly to nociceptive pain in emotional and cognitive processing
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Nerve blocks are usually not effective, anticonvulsants may be trialled if pain is neuropathic, tricyclics help in facial pain
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The definition covers amnesia, fugues and psuedoseizures
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Dissociative disorders require the following 3 characteristics:
1) They occur in the absence of physical pathology that would explain the symptoms

2) They are produced unconsciously
3) Symptoms are not caused by over activation of the nervous system
Other characteristics: childhood trauma, may reflect patient’s ideas about illness, social advantage of being ill, accompanying
physical disease
...


Other examples of functional somatisation disorders:
•
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Tension type headaches – mild/moderate, bilateral, non pulsating, not aggravated by anything, no nausea/vomiting
Atypical face pain or chest pain
Fibromyalgia
Chronic regional pain syndrome
Chronic fatigue syndrome
Multiple chemical sensitivity
Pre-menstrual syndrome
Irritable bowel/bladder

2) Headaches and facial pains, including approaches to severe headaches

Duration
+2 or more of
...

Always unilateral
Always on the same side
Watery, blood shot eyes
...

Excruciating pain around the eye
Acute; 100% 15L O2 via non-rebreather +6mg
sumatriptan

Warm/cold packs to head
If no effect in 2 months can try Beta blockers e
...
propanolol
Stop caffeine, drugs, alcohol,
Try exercise, hydration, regular meals, regular sleep

Preventative: temporary injectable steroids
(prednisolone) until the verapamil starts to work
as can take a few days
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Alcohol= trigger

Headaches can be primary (trigeminal, medication overuse, tension, migraine) or secondary (high/low pressure, mass/lesions,
vascular, SAH, meningitis)
Have you ever had a headache before?
flags:

Red
Yes

No

What was the original headache
like?

How did your headache start?
Acute or progressive?

Do they still happen?
What is the current one like?
Are there any days without a
headache?
Do you take any analgaesics?

is it daily or does it come and
go?

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New onset >50yrs/cancer/
•
Thunderclap (SAH)
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Focal neurological symptoms/abnormal
signs
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Change in frequency or characteristics
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Changes with posture
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Worse on coughing/ laughing/ straining
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Neck stiffness/fever

Are there any triggers?

Deendency? - type and how
often
Life style --> sleep, caffeine,
H2O, food, alcohol, smoking?

decscription of headache,
additional symptoms

Are there any red flags?

description of headache,
additional symtoms

Chronic daily headache – defined as headaches on more than 15 days per month for more than 3 months
...
This is to stop medication overuse headaches
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After 3 weeks their headaches should improve
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For coping with withdrawal symptoms: NSAIDs for a few days only, anti-emetics, ice/cooling strips, rest, anti anxiety meds
(anxiolytics)
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Continue lifestyle changes and start preventative treatment
...
Now they use medication to
‘keep going’ and are having a daily migraine in middle age
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Same treatment as chronic daily headache
It is a complication of other headaches so it is hard to know the underlying cause until painkiller stopped

Chronic migraine – the choice of drug is determined by the side effect profile
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Hemicrania continua – continuous unilateral headache of moderate intensity with occasional short, severe episodes
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There may also be eye redness, nasal dripping, ptosis, miosis (contracture of the
iris)
...
BU

Hypnic headache – elderly, nighttime usually, uni or bilateral but no additional features
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Indometacin, methysergide

Facial pain:
Trigeminal neuralgia – usually starts in the 50s/60s
...
There are no signs of Vth nerve dysfunction on examination
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It is usually caused by compression of the trigeminal nerve at or near the pons by a blood vessel
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Presentation is paroxysmal knife like or electric shock pain in face
...
spontaneous remissions last months or years before relapse
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If this fails then surgery to relieve the nerve
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No associated features, continuous and variable
...
Treatment is with Gabapentin,
amitryptiline, tramadol, oxycodone, lignociane patch
...
There is
not findings or pathology and nothing helps
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Often a burning sensation with the area being sensitive to touch, along with pins and needles
...


3) Transient loss of consciousness – e
...
TIAs, epilepsy, transient
focal neurological deficits, cervical cord lesions, going off legs’
Always ask yourself
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Absence seizures,
atonic seizures and
myoclonic jerks are
shorter
...

Tongue biting,
incontinence and sore
muscles/headache
after

Older patients
...
More
common in men
Negative symptoms:
numbness, visual loss,
paralysis, ataxia
...
E
...

scomatoma followed
by parasthesia

20-30 mins

Any age, usually
younger
More common in
women
Light headed, dim
vision, decreased
alertness
...
You can also get
compression of vascular structures or obstructive hydrocephalus
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Functional disorders – hoover’s sign is a test for if this is a functional disorder
...
At
the same time try and push up their other leg without telling them
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Cerebrovascular disease – “a clinical syndrome consisting of rapidly developing clinical signs of focal disturbance of cerebral
function lasting >24hrs or leading to death with no apparent cause other than vascular origin
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In a posterior cerebral
artery stroke the patient
will experience homonymous
hemianopia (loss of half the field of
view on the same side of both eyes)
and alexia without agraphia (patients
can still write but are unable to read)
...
Seizures are due to abnormal electrical activity in the brain
...

It can be classified into primary generalised (when the electrical activity starts in both hemispheres) or partial (when it starts in a
focal part of the brain
...
g
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In secondary generalised epilepsy the focal
symptoms may precede the generalised seizure and are called ‘auras’
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Unilateral weakness (Todd’s palsy) indicates a focal motor
cause
...

•
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Reflex anoxic seizures – look like tonic clonic
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Low BP – LOOK FOR CARDIAC CAUSES

The epilepsy history:
1
...

3
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Tongue biting and a long recovery post-ictally are very suggestive of epilepsy
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Are there any triggers? – alcohol, stress, certain sounds, flashing lights…
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Flaccid suggests vagovagal
Any injuries – tongue biting is suggestive of seizure
Any incontinence – faecal especially, urinary is non specific
Any colour change – green suggests vago vagal
How soon did the patient come around – epilepsy usually a while

Is this the first ever seizure? – the patient may recall episodes of de ja vu or funny turns
...

Investigations: CT/MRI to rule out other intracranial lesions, EEG to check for seizure activity, bloods to check for electrolyte
disturbance
...
Usually have an aura which reflects origin
and initial spread
...
They have focal motor or sensory symptoms
with no post ictal symptoms
...

Awareness is impaired
...
There is evidence of focal start on the
EEG
Electrical discharge throughout the cortex
...
Often in childhood/adolescence and with no warning
...
E
...
suddenly stops talking and then carries on where left off
Sudden jerk of limb face of trunk
Ridged (tonic) phase followed by jerk (clonic)
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Parietal
lobe leads to sensory disturbances
...

2
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4
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Vascular – AV malformations, stroke, post stroke
Infective – fever, TB meningitis, meningoencephalitis
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7
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9
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Idiopathic/congenital – epilepsy
Neoplasm
Syndromes - Tuberous sclerosis, Down’s, Von Hippel Lindau
pSuedoseizures
drugs – tricyclics, cocaine, tramadol, theophylline

Driving – the patient should not drive for 1 year post seizure
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Treatment: withdrawal can be considered if seizure free for 2yrs+
...

treatment is started only after firm diagnosis of epilepsy or after 1st seizure if there is a high chance of recurrence
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If medication needs to be changed the second is added in slowly and then they are
weaned off the first
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warn about the interaction of some AEDs with the OCP
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A higher dose Combined OCP is recommended
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The risk of the AED may be outweighed
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Explain about the teratogenicity, Sodium Valporate especially
...
AFP
measurements should be taken
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Status epilepticus
Prolonged seizure for 20mins +
Treatment:
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•
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Secure airway (ABCDE)
High flow oxygen
Check glucose level

•

Establish IV access – give 4mg IV lorazepam
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*TEN = toxic epidermal necrolysis – rare life threatening skPhenytoinin condition due to drug reaction
...
Mortality 30% )steven Johnson syndrome
*in women of child bearing age use lamotrigine instead of sodium valproate
In general → Partial = carbemazipine, General = sodium valproate or lamitrigone

Blackouts: what does the patient mean by blackouts? It could be loss of consciousness or blurring vision, diplopia or vertigo
...
Fear, pain and
prolonged standing are the main causes
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There is arapid recovery and
no symptoms post syncope so distinguishable from a faint
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Other – hypoglycaemia, weak legs(elderly), ficticious, anxiety, choking

Spinal cord compression

Back pain red flags:
•

Features – previous malignancy, <16 or >50 with NEW onset, weight loss,
recent serious illness or infection
Signs – saddle anaesthesia, reduced anal tone, urinary retention, hip oir
knee weakness, generalised neurological deficit
Symptoms – non-mechanical pain worse at rest
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Cord compression – back pain, leg weakness, limb numbness, ataxia,
urinary retention with overflow, hyper-reflexia, clonus, extensor plantar

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80% will suffer with back pain, 50% for >24hrs
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L4/5 and L5/S1 are most common
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Spinal stenosis produces the typical spinal claudication (when walking) leg pain
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•

Signs of spinal cord compression: spasticity, limb weakness, brisk reflexes, externsor platar, sensoryt loss, local signs

•

Fractures
o

Are they stable or unstable?

o

The spinal column is divided into 3: the anterior column (Anterior longditudinal ligament and the anterior ½ of
the vertebral body), middle column (posterior ½ of body and post
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Spondylolisthesis – when one of the vertebrae slips forward or backward
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•

Syringomyelia – fluid filled cavity within the NS

•

Tumours
o

They can be classified into 3: Extradural,
intradural extramedullary and intra dural
intramedullary

o

intradural extramedullary – inside the dura,
under the membrane that covers the cord but
outside the nerves e
...
meningioma or
schwannomas

•

•

o

intradural intramedullary – grow from inside the spinal cord or inside the individual nerves
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o

Para/tetraplegia

Vascular – is this acute bleed or blackage
...
Most are caused

Figure 1SAH

by aneurysm and then trauma
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Also weaker walls
▪

•

Treatment – warfarin, clopidigrel, aspirin, NOACs

Tumours – Primary/ secondary, benign/malignant, intra-axial/extra-axial
Figure 2Subdural

Hydrocephalus – increase in CSF and ventricular dilation
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•

PC – headache, being sick, blurred vision, papilledema
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Head injury - 1
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Use ABC and avoid hypoxia and hypotension
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40%mortality

Figure 3Extradural

Transient focal neurological deficits:
Gait apraxia – loss of ability to execute activity
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Increasing signs of parkinsonism
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Lesions of prefrontal/parietal lobes
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Gait Ataxia – there is loss of coordination of muscles
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4
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The two types of disorder are the Akinetic-Rigid syndromes (slowed movement and increased tone) or dyskinesia (added
uncontrollable movements)
Akinetic rigid syndromes:
Hypokinetic = parkinsons
Hyperkinetic:
→ Tic
→ Tremor – involuntary oscillation of a body part
...


o
o

→
→
→

Resting tremor – e
...
parkinsonian
Postural tremor – when a body part is maintained in a posture e
...
essential tremor
...

▪
Essential tremor is also known as benign essential tremor
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Symmetrical
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Intention tremor – when the action is goal directed e
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cerebellar
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Also in essential tremor, cluster
headaches and psychiatric disorders
MND – has LMN wasting and UMN brisk reflexes
...
Chorea and personality change precede
dementia and death
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Parkinson’s
In the absence of dopamine, the SN still receives inhibiting signals from the cholinergic stimulation (Ach)
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The 3 characteristic features are tremor, rigidity and bradykinesia
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Cog wheel is due to the combined tremor and rigidity
Bradykinesia – causes the shuffling gait
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Blank, expressionless face
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There is an increase in tendon jerks

Non-motor symptoms include fatigue, dementia, depression, constipation, poor sleep
...
Dopamine cannot pass through the BBB but LD can
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Dopa de-carboxylase inhibitors are given with L-Dopa to prevent peripheral side effects
...
The nausea and vomiting caused by L-Dopa is treated with domperidone (dopamine antagonist
that does not cross the BBB)
Limitations of L-Dopa therapy:
•
•
•
•

Reduced effectiveness over time even with increasing the dose
LD induced dyskinesis
On-off effect -0 fluctuations between normal functions and restricted mobility
The duration of each dose becomes shorter over time

Parkinson’s:
•

Parkinson’s is when there is loss of dopamine secreting cells in the substantia nigra
...
Typical onset is 65+
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Causes: mostly unknown
...
Genetic factors
found in early onset
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Clinical features:
1) Resting tremor – made worse by anxiety and improved by voluntary movement
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The limbs resist passive extension through movement
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The face is expressionless, speech is slow and monotonous
4) Postural changes – stoop, gait shuffling, poor balance
...
Often given with Carbidopa
which inhibits dopadecarboxylase in the periphery
...
Side effects: nausea and vomiting
...

▪
Side effects: Hypotension, nausea, dyskinesia
3) Entacapone – COMT inhibitor
...

4) MAO-B inhibitors – selegline – alternative to dopamine agonists in early PD
5) Surgical for advanced disease – once experiencing freezing wpisodes and completely dependent on Ldopa
▪
Deep brain stimulation
▪
Apomorphine infusion (dopamine infusion)

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MS
Discrete plaques of demyelination occur at multiple CNS sites – T cell mediated response
...


•
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• To diagnose there must be 2 episodes separated by time and space
• Symptoms are worse on heat – can present with optic neuritis, numbness, leg weakness
• Poor prognosis if motor symptoms present at diagnosis
Brain and spine MRI – demyelination shown
...
Do to rule out other things
...

Management:
o Physio
o Steroids – methyl prednisolone can shorten relapses
o Interferons – can reduce relapses but does not delay disability
...


Optic neuritis is common presentation

5
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3 = dead

6
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Vertigo is always worsened by movement
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There are 5 organs of balance in each ear;
•
•

3 semicircular canals – these are angular and have hair cells organised under copula
utricle and saccule – these are called the Otolothic organs and are linear
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The vestibular nerve has 2 branches, an inferior and superior
...
The goal of vertigo treatment is to restore the balance
between the 3 inputs
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There may be pallor and
sweatiness and nausea and vomiting
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If there is loss of awareness in the attacks, then it is probably not vertigo and differentials should be epilepsy or syncope
...
!!!! These are the same as acoustic neuroma!!!
▪ Treat with salt restriction and diuretics – disease due to salt and water disturbance
o Vestibular neuritis
▪ Sudden onset of peripheral vertigo without hearing loss
...
Spontaneous, treatment
aimed at stopping inflammation
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Of hearing loss occurs then
may need referral to ENT
...
It is a problem with the posterior SCC and there are calcium deposits
...

▪ Diagnosis – Hallpike manoeuvre – stand to the side of the patient and turn their head towards you
...
Keep their eyes open and repeat on the other side
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▪ Treatment: epley manoeuvre – involves head movements to reposition ‘crystals’ that are causing the
vertigo
...


The most common treatment is Prochlorpromazine – stemital

7
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Delirium, Dementia, Developmental disability, Deficit, Depression, Delusional state, Dissociative
state
...
Consciousness fluctuates, unlike in dementia!
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It occurs in around 15% of elderly patients in hospital
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Causes: Infection and drugs are the main causes
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Maintain patient safety and sensory environment
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o Often Haloperidol is the drug of choice, along with lorazepam and olanzapine
Disordered thinking – slow, irrational ideas
Euphoric, fearful, depressed or angry
Language impaired
Illusions, delusions, hallucinations
Reversal of sleep wake cycle
Inattention – focussing or sustaining attention is poor
Unaware/disorientated
Memory deficits
...

•

Affects 10% over 65 and 20% over 80
...
Lewy Body, Pick’s disease, Huntington’s
...

Apraxia – difficulty in planning or initiating task
...


Stroke:
First the limbs are flaccid and then become spastic
There are 2 main types – haemorrhagic (15%) and infarction (85%)
A stroke due to infarction shows up as a black area of low density on the CT, with a surrounding white area due to cerebral
oedema
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The management of haemorrhagic and infarction differs so it is important to differentiate the two
...
If the CT shows infarction give aspirin 300mg daily
If the patient presents within 4 ½ hours of confirmed symptoms and is confirmed infarction, then they can be thrombolysed
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Initially following a stroke the BP may be high due to disturbance of cerebral autoregulation and should therefore should not be
treated in the acute phase in case it impairs cerebral perfusion
...
, It will disrupt autoregulation and may decrease cerebral perfusion

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