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451
https://t.me/med1917
10 Neurology
Fig 10.
7
Posterior view.
Fig 10.
8
The anterior ⅓ of the scrotum is
L1
; the posterior ⅔ is S3. The penis is
at its root).
S2/ 3 (L1
Fig 10.
9
Feet and hands.
10 Neurology
Headache
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452
Every day, thousands of people visit the doctor complaining of headache. Headache
is divided into primary (predominantly migraine, tension- type headache and the trigeminal autonomic cephalgias) and the much rarer secondary syndromes that must
be excluded (space- occupying lesions, meningitis, subarachnoid haemorrhage).
Onset Rapid onset The key diagnosis to rule out here is: •Subarachnoid haem-
SAH
, p
474
orrhage (
): sudden- onset, ‘worst ever’ headache, often occipital, sti neck,
focal signs, consciousness. Other dierentials include:
striction syndrome: often recurrent ‘thunderclap’ headaches mimicking
include physical exertion, sex, swimming, Valsalva, usually benign but beware stroke
•Meningitis (p
risk.
LP
, start antibiotics. •Encephalitis (p
sciousness. Do an urgent
genic after
806
LP
or epi dura l ana esth esia , or s pont aneo us (m ost l ikel y spi nal
sometimes after minor trauma or a sudden sneeze). Suspect if headaches worse on
standing.; treat with epidural blood patch over leak, if conservative management
with hydration and caeine fails.
to the dissected artery that is usually progressive but can be rapid onset. Look for
Horner’s, pulsatile tinnitus, anterior (carotid) or posterior (vertebral) territory stroke.
Character Tight band/ dull pressure sensation •Tension- type headache: the usual
cause of bilateral, non- pulsatile headache ± scalp muscle tenderness, recognized
as a separate condition but increasingly considered as mild/ moderate migraine.
Throbbing/ pulsatile/ lateralizing •Migraine (p
Frequency Continuous pain (chronic daily headache) •Chronic migraine (p
•Medication overuse headache (see ‘Drug history’). •Hemicrania continua (strictly
unilateral, autonomic features, responds to indometacin).
ache over frontal or maxillary sinuses, with tenderness ± postnasal drip. Pain is
worse on bending over.
most days •
ache’).
Migraine. •Trigeminal autonomic cephalgias (see
•Trigeminal neuralgia (see
Duration Chronic, progressive headaches can indicate
waking, lying, bending forward, or coughing. Also: vomiting, papilloedema, seizures,
false localizing signs, or odd behaviour. Do imaging to exclude a space- occupying
lesion, and consider idiopathic intracranial hypertension.
ICP
due to the risk of cerebellar herniation.
acute
Associated features Eye pain ± reduced vision •Acute glaucoma. Typically eld-
erly, long- sighted people. Constant pain develops rapidly around one eye, radiating
to the forehead with markedly reduced vision, visual haloes, and a red, congested
p
559
). Seek expert help at once. If delay in treatment of >1h is likely, give
eye (
eye drops (eg
PO.
Jaw claudication, tender scalp with thickened, pulseless temporal arteries
Giant cell arteritis (p
•
in all >
0.5
% timolol maleate ± 2% pilocarpine) and acetazolamide
50
yrs old with a headache that has lasted a few weeks: prompt diagnosis and
steroids avoid blindness.
Precipitating causes Head trauma Commonly causes localized pain but can be
more generalized. It lasts ~
dural or extradural haemorrhage if drowsiness ± lucid interval, or focal signs (
Also ask about Analgesia, sex, food (eg chocolate, cheese, coee).
Drug history •Medication overuse headache: culprits are mixed analgesics (para-
cetamol + codeine/ opiates), ergotamine, and triptans ≥
common reason for episodic headache becoming chronic daily headache. Analgesia
must be withdrawn— aspirin or naproxen may mollify the rebound headache. A preventive may help once o other drugs (eg tricyclics, valproate, gabapentin;
Limit use of over- the- counter analgesia (no more than
Social history Ask about stress or recent life events; may not explain the path-
ology, but will help you appreciate the context in which symptoms are experienced.
•Reversible cerebral vasocon-
SAH
, triggers
): fever, photophobia, sti neck, purpuric rash, coma. Do an
808
MRI
and LP •Intracranial hypotension:
): fever, odd behaviour, fits, or reduced con-
CSF
leakage, eg iatro-
CSF
leakage,
•Cervical artery dissection: headache ipsilateral
454
).
454
•Sinusitis: dull, constant
CT
can confirm diagnosis but is rarely needed. Pain- free
BOX
‘Trigeminal neuralgia’).
BOX
‘Cluster head-
ICP
. Typically worse on
LP is contraindicated in
500
554
): subacute- onset headache with
2
wks; often resistant to analgesia. Do CT to exclude sub-
ESR
>40mm/ h. Exclude
3
d per week. This is a
6
d per month).
p
p
476
500
).
mg
).
).
Cluster headache and other trigeminal autonomic cephalgias
SUNCT
MRI
https://t.me/med1917
The trigeminal autonomic cephalgias (
TAC
S) are a group of primary headache dis-
orders that involve activation of the trigeminal and parasympathetic systems,
characterized by short- lasting unilateral pain with variable ipsilateral cranial
autonomic features. The cause of these is unknown.
Cluster headache The most common, and may be the most disabling of the pri-
5:1
mary headache disorders. : ≥
Symptoms: rapid- onset of excruciating pain around one eye that may become
watery and bloodshot with lid swelling, lacrimation, facial flushing, rhinorrhoea,
miosis ± ptosis (
fects the same side. Agitation is typical during attacks, in contrast with migraine.
It lasts
4– 12
last
fore the next cluster.
100
% O2 for ~15min via non- rebreathable mask (not if
6
mg at onset (or zolmitriptan nasal spray 5mg). Preventives: avoid triggers, eg
20
% of attacks). Pain is strictly unilateral and almost always af-
15– 180
min, occurs once or twice a day, and is often nocturnal. Clusters
wks and are followed by pain- free periods of months or even 1– 2yrs be-
Treatment: acute attack ‘Keep calm ... carry oxygen’: give
alcohol. Medication: verapamil (
consider: corticosteroids (short term only; many
; onset at any age; commoner in smokers.
COPD
); sumatriptan SC
360
mg in three divided doses) is first line. Also
SE
); topiramate; lithium (monitor
carefully).
Paroxysmal hemicrania Shorter duration (2– 30min) and more frequent attacks
than cluster headache (up to
/ d). Like hemicrania continua (another
TAC
40
sponds to indometacin treatment; a treatment trial is so easy so consider this!
Short- lasting unilateral neuralgiform headache with conjunctival injection and tearing (
) The longest name but the shortest duration (seconds–
minutes) and the highest frequency (up to hundreds/ day) of attacks.
Trigeminal neuralgia
Symptoms Paroxysms of intense, stabbing pain, lasting seconds, in the trigem-
inal nerve distribution. It is unilateral, typically aecting mandibular or maxillary
divisions. The face screws up with pain (hence tic douloureux).
Triggers Washing aected area, shaving, eating, talking, dental prostheses.
Typical patient >50yrs old; in Asians : ≈ 2:1.
Secondary causes Compression of the trigeminal root by anomalous or aneur-
ysmal intracranial vessels or a tumour, chronic meningeal inflammation,
skull base malformation (eg Chiari).
This is necessary to exclude secondary causes (~
: Carbamazepine (start at
200– 400
toin
cessary. This may be directed at the peripheral nerve, the trigeminal ganglion,
mg/ 24h PO; or gabapentin (p
100
mg/ 12h PO; max
500
% of cases).
400
mg/ 6h; lamotrigine; pheny-
). If drugs fail, surgery may be ne-
MS
or the nerve root.
Microvascular decompression Anomalous vessels are separated from the
trigeminal root. Stereotactic gamma knife surgery can work, but length of pain
relief and the time to treatment response are limiting factors.
Facial pain : p61.
453
10 Neurology
), it re-
, zoster,
10 Neurology
Migraine
CHOCOLATE
https://t.me/med1917
454
15
% of us suer from migraines, (:
other neurological conditions combined.
Symptoms Prodrome Premonitory symptoms hours/ days before headache are
present in the majority: tiredness, yawning, mood/ concentration change.
Reversible neurological symptoms are present in a third, usually of gradual onset,
resolves typically within an hour. Usually precede the headache, but may accom-
• Visual: chaotic distorting, ‘melting’ and jumbling of lines, dots, or zigzags,
pany it.
scotomata or hemianopia.
• Motor: dysarthria and ataxia (migraine with brainstem aura), ophthalmo-
to face.
plegia, or hemiparesis. (
much more common.)
aura with no headache can occur.
ache, typically aggravated by head movement or physical activity. Median duration
24
h. Accompanying neck pain, nausea, vomiting ± photophobia/ phonophobia is
is
common. There may be allodynia— all stimuli produce pain: ‘I can’t brush my hair,
wear earrings or glasses, or shave, it’s so painful.’
toms similar to those listed in the prodrome, usually lasting <
Partial triggers Seen in 50%:
cheese/ caeine, oral contraceptives, lie- ins, alcohol, travel, or exercise.
Diagnosis Clin ical, b ased on the histor y. Diagnostic criteria if no aura ≥5 headaches
4– 72
lasting
• Pulsating • Impairs (or worsened by) routine activity.
h + nausea/ vomiting (or photo/ phonophobia) + any 2 of: • Unilateral
Dierentials Cluster or tension headache, cervical spondylosis, BP, intracranial
pathology, sinusitis/ otitis media, dental caries.
Acute management Inadequate acute treatment is associated with progression
to chronic migraine.
1 Triptans have strong evidence for eectiveness, and may be
improved by combination with
alone in mild to moderate attacks). Evidence on stroke risk with triptan use is conflicting; use cautiously if there is a prior history of vascular events. Rescue
may be useful in emergency department presentations, eg metoclopramide
Preventive management Can achieve ~50% in attack frequency in most pa-
tients; consider after risks and benefits discussion.
Avoid identified triggers (a headache diary can help) and ensure analgesic
apies
rebound headache is not complicating matters (
lation may help.
25– 50
mg/ 12h (teratogenic, can interfere with
Medications 1st line: Propranolol 40–
nocte can be used, though this is o licence. Patients may be on previously recommended prophylactic agents (eg valproate, verapamil, pizotifen, pregabalin, or
i/ARB): if achieving good control then continue as required.
been approved for migraine prevention for patients with at least
per month who cannot tolerate or who have not achieved control with
preventive treatments (see
injections are a last resort in chronic migraine.
Considerations in females Incidence of migraine (especially with aura) + is-
chaemic stroke is increased by use of a combined
non- hormonal contraception in migraine + aura, though a low- dose combined
can be used in those without aura. Further risk:
• Obesity (body mass index >30). • Diabetes mellitus. • Hyperlipidaemia. • Family
history of arteriopathy <
aura or worsening migraine; see
or triptans on the days migraine is expected.
if not, get help— worsening headaches in pregnancy are associated with a greater
risk of pre- eclampsia and cardiovascular complications. Oer paracetamol
Triptans and
NSAID
S can be used but discuss risks and benefits with patients first.
Don’t use aspirin if breastfeeding. Anti- emetic: metoclopramide (up to
or promethazine. Prophylaxis: seek specialist advice.
3:1
); responsible for more disability than all
Aura
• Somatosensory: paraesthesiae spreading from fingers
Hemiplegic migraine is rare; misdiagnosed
TIA
/ stroke is
• Speech: (8% of auras) dysphasia or paraphasia. • Isolated
Migraine headache Unilateral, throbbing head-
Postdrome Occurs in 80%, symp-
12
NSAID
or: chocolate, hangovers, orgasms,
TIA
S may mimic migraine aura.
S/ paracetamol (the latter should be first tried
h.
IV
therapy
10
mg.
Non- pharmacological ther-
p
452
). Transcutaneous nerve stimu-
120
OCP
BOX
‘Stolen moments’). 12- weekly botulinum toxin type A
mg/ 12h or topiramate
ecacy). Amitriptyline 10– 75mg
2– 3
ACE
previous
OCP
CGRP
antagonists have
4
headache days
OCP
. Use progesterone- only or
• Smoking. • Age >35yrs. • BP.
45
yrs. Warn patients to stop
OHCS
p
153
. Perimenstrual migraine Consider
OCP
at once if they develop
Pregnancy Migraine often improves;
NSAID
1
st line.
5
days only)
-
S
Stolen moments
https://t.me/med1917
Decades after any hope of its safe return
had been extinguished, along with the life
of its former virtuoso owner, a stolen
Stradivarius violin was recovered from
a dusty Californian attic in
ticulously restored. Snatched by a former
student after a lesson, the Totenberg
Stradivarius (
its life immured in darkness, ceding its
fig
10.10
) spent 35 years of
2015
1734
and me-
rich velvet voice for uninterrupted silence.
After a similar painstaking search, chronic
migraine is finally giving up its secrets.
There is renewed hope that precious moments callously stolen from migraineurs,
relegated to silent darkness by piercing
dissonance, might gradually be returned.
The previously favoured theory of dilatation of meningeal arteries as the root
Fig 10.
10
The Totenburg Stradivarius.
Artwork by Gillian Turner.
cause has been largely disproved. Rather, neurogenic inflammation of trigeminal
sensory neurons caused by cortical spreading depression modulates how pain
is processed and also results in aura. The calcitonin gene- related peptide (
discovered in the
tation and pain transmission.
or its receptor are approved for migraine prevention, and oral
1980
s, has been found to play a key role by mediating vasodila-
IV
monoclonal antibodies directed against
CGRP
CGRP
CGRP
antagonists
(‘gepants’) are eective for acute management and for prevention. They have not
been studied in pregnancy, and should be avoided for now in people with recent
ischaemic events, since
CGRP
has theoretical cardioprotective eects.
455
10 Neurology
),
10 Neurology
Blackouts
https://t.me/med1917
456
Causes of collapse ± loss of consciousness (
BOX
‘Blackout history’).
(see
Vasovagal (neurocardiogenic) syncope Occurs due to reflex bradycardia ± per-
ipheral vasodilation provoked by emotion, pain, or standing too long (it cannot occur
when lying down). Onset is over seconds (not instantaneous), and is often preceded
by pre- syncopal symptoms, eg nausea, pallor, sweating, and narrowing of visual
fields. Brief clonic jerking of the limbs may occur due to cerebral hypoperfusion,
but there is no tonic/ clonic sequence. Urinary incontinence is uncommon, and there
is no tongue- biting. Unconsciousness usually lasts for <
Situational syncope Symptoms as for vasovagal syncope but with a clear precipi-
cough syncope occurs after a paroxysm of coughing; effort syncope is brought
tant:
on by exercise; there is usually a cardiac cause, eg aortic stenosis,
happens during or after urination: mostly men, at night.
syncope
Carotid sinus syncope Hypersensitive baroreceptors cause excessive reflex brady-
cardia ± vasodilation on minimal stimulation (eg head- turning, shaving).
Epilepsy (p
486
) Features suggestive of this diagnosis include: attacks when asleep
or lying down; aura; identifiable triggers (eg
tonic– clonic movements; incontinence of urine; tongue- biting; prolonged post- ictal
drowsiness, confusion, amnesia, and transient focal paralysis (Todd’s palsy).
Stokes– Adams attacks Transient arrhythmias (eg bradycardia due to complete
heart block) cause cardiac output and
with no warning except palpitations; injuries are common), and is pale, with a slow
or absent pulse. Recovery is in seconds: the patient flushes, the pulse speeds up, and
consciousness is regained. As with vasovagal syncope, anoxic clonic jerks may occur
in prolonged
LOC
. Attacks may happen several times a day and in any posture.
Other causes Hypoglycaemia (p
LOC
headedness or
LOC
on standing from lying in those with inadequate vasomotor reflexes: the
or
; rare in non- diabetics. Orthostatic hypotension Unsteadiness
elderly; autonomic neuropathy (
multisystem atrophy (
tachycardia, paraesthesiae, light- headedness, and no
Drop attacks Sudden fall to the ground without
leg weakness but may also be caused by hydrocephalus, cataplexy, or narcolepsy.
Psychog enic
Pseudosyncope, non- epileptic seizures (p
Examination Cardiovascular, neurological. Measure BP lying and standing.
Investigation
urgently if associated with palpitations, arrhythmias,
longed
U&E, FBC
brain;
ECG
: all with recurrent syncope (or falls) need cardiac assessment—
QT
interval (p
2
+
2
, Mg
ABG
+
, Ca
, glucose; tilt- table test;3
if practical (PaCO2 in attacks suggests hyperventilation as the cause).
While the cause is being elucidated, advise against driving (see p
Transient global amnesia
Characterized by a sudden onset of anterograde amnesia (the inability to form new
memories) lasting up to
for the duration of the episode. The cause is uncertain, but hippocampal diusion-
MRI
weighted
clude physical exertion, sex, emotional events, and cold- water exposure. There is
disorientation in time and place (but not person), often prompting repetitive questioning, but semantic memory is preserved.
Management Reassurance; there is no increased risk of stroke, episodes do not
usually recur, and no driving restrictions apply. Frequent recurrences or occurrence
on waking should prompt investigation for epileptic amnesia.
lesions are common, suggesting a vascular mechanism. Triggers in-
LOC
) are many; take a careful history
2
min and recovery is rapid.
HCM
TV)
; altered breathing; cyanosis; typical
LOC
. The patient falls to the ground (often
208
) Tremor, hunger, and perspiration herald light-
p
501
); antihypertensive medication; over- diuresis;
; p
490
). Anxiety Hyperventilation, tremor, sweating,
ECG
(arrhythmia, long QT, eg Romano– Ward, p88);
LOC
suggest a panic attack.
LOC
. Mostly benign and due to
460
), Münchausen’s (p
3
rd- degree AV block, or pro-
EEG
, sleep
EEG
; echocardiogram;
697
MSA
) ± 24h
150
24
h, with full recovery except for a ‘blackout’ of memory
; micturition
694
).
CT/ MRI
).
Blackout history
https://t.me/med1917
Talk to the patient and witnesses and let them tell you as much as possible
without prompting or leading. Ask:
Before the attack
• Is there any warning?— Eg epileptic aura or pre- syncopal symptoms.
• In what circumstances do attacks occur?— Eg posture (standing/ sitting/ supine),
exertion, if watching
• Can the patient prevent attacks?
TV
con sider epile psy.
During the attack
• Does the patient lose awareness?
• Does the patient injure themselves?
• Does the patient move? Are they sti or floppy? (A tonic phase preceding clonic
jerking points towards epilepsy.)
• Is there incontinence? (More common in epilepsy, but can occur with syncope.)
• Does their complexion change? (Pale/ cyanosis suggests epilepsy; very pale suggests
syncope or arrhythmia.)
• Does the patient bite the side of their tongue? (Suggests epilepsy.)
• Are there associated symptoms, eg palpitations, sweats, pallor, chest pain,
• How long does the attack last?
dyspnoea (
fig
10.11
)?
After the attack
• How much does the patient remember about the attack?
• Is there muscle ache? (Suggests a tonic– clonic seizure.)
• Is the patient confused or sleepy? (Suggests epilepsy.)
Background to attacks
• When did they start?
• Are they getting more frequent?
• Is anyone else in the family getting them? Sudden arrhythmic death may leave no
evidence at postmortem, or there may be hereditary cardiomyopathy (refer those
with a relative who has had a sudden unexplained death <
40
yrs old).
457
10 Neurology
Fig 10.
11
VT causing blackout in Brugada syndrome (p
with an implantable defibrillator (
The dying of the light
People reporting that they have ‘blacked out’ may be inadvertently condemning
themselves to the title of ‘poor historian’; a lamentable part of the medical lexicon
that ought to be expunged, not least because it is misaddressed (a historian records
history). Why should we expect the storyteller to be able to clearly characterize the
absence of something intangible? The light is extinguished for around a third of our
lives, but even the most eloquent of us would be hard- pressed to begin to explain
what we lose during the daily disconnect from our external world. The loss of light
may be literal (amaurosis fugax,
of independence (falls,
3
Patient is subject to continuous
resting horizontal position to vertical. Induction of symptoms with inappropriate
bradycardia suggests neurally mediated syncope. Consider pacing.
p30), or all- encompassing (syncope, seizures).
687
p
128
).
p
469
), metaphorical (transient amnesia), symbolic
ECG
and BP monitoring while strapped to a table and moved rapidly from
). This patient had been treated
BP
drop >30mmHg or
10 Neurology
Vertigo and dizziness
BPPV
TIA
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458
Is this vertigo? Complaints of ‘dizzy spells’ are very common and are used by pa-
tients to describe many dierent sensations. True vertigo is a hallucination of movement, often rotatory (
tilt, sink, or rise. The key to diagnosis is to find out exactly what the patient means by
table
10.7
). In practice, simple ‘spinning’ is rare— the floor may
‘dizzy:’ if this is not vertigo or if atypical symptoms are present consider other causes,
eg if there is loss of awareness, think of epilepsy or syncope; if there is faintness, lightheadedness, or palpitations, think of anaemia, dysrhythmia, anxiety, or hypotension.
Table 10.
7
Causes of vertigo by time course and associated features
Cause Duration Characteristics
Benign
positional
paroxysmal
vertigo
(
Posterior
circulation
Ménière’s
disease
Migraine
with
brainstem
aura
Vestibular
neuronitis
Posterior
circulation
stroke
Recurrent
episodes,
seconds/
minutes
)
Single or
recurrent,
minutes/
hours
Recurrent
episodes,
minutes/
hours
Recurrent
episodes,
minutes/
hours
Single
episode,
hours/
days
Single episode, days/
weeks
Provoked by changes in head position due to disruption of
debris in the semicircular canal of the ears (canalolithiasis).
Fatiguable nystagmus on performing the Hallpike manoeuvre
is diagnostic; Epley manoeuvres clear the debris (
See stroke, below. Requires urgent assessment and
treatment; the risk of early recurrent stroke may even be
greater than that for anterior circulation
Increased pressure in the endolymphatic system of the inner
ear causes recurrent attacks of fluctuating (or permanent)
sensorineural hearing loss, and tinnitus (with a sense of aural
fullness ± falling to one side ). : bed rest and reassurance in
acute attacks. An antihistamine (eg betahistine) is useful if
prolonged, or buccal prochlorperazine if severe, for up to
History of migraine, migraine triggers (
Viral/ post- viral inflammation of the vestibular nerve; often
preceded by upper respiratory viral infection. Abrupt onset of
severe vertigo, nausea, vomiting ± prostrat ion. Call ed ‘labyr inthitis’ when associated with hearing loss. Severe vertigo subsides
in days, complete recovery takes
Usually accompanied by other symptoms (weakness,
dysarthria, dysphagia, diplopia, nausea/ vomiting, ataxia),
but even isolated vertigo can be caused by ischaemia
p
454
3– 4
wks. : reassure. Sedate
TIA
OHCS
p
405
)
7
)
d
Others MS; ototoxicity (aminoglycosides, loop diuretics, aspirin and cisplatin can
cause deafness ± vertigo); trauma to petrous temporal bone; motion sickness (mal
de débarquement); herpes zoster of the external auditory meatus; facial palsy ± deaf-
ness, tinnitus, and vertigo (Ramsay Hunt syndrome, see
Tinnitus
This ringing or buzzing in the ears is common, and may cause depression or insomnia.
Investigate unilateral tinnitus fully to exclude an acoustic neuroma (p
Causes Sensorineural hearing loss (leading to auditory cortex hyper- excitability),
excess noise, head injury, ototoxic drugs, otitis media, Ménière’s. If
vascular causes (carotid stenosis/ dissection,
Management Often a chronic condition; the goal is to lessen the impact and manage
associations (depression, insomnia) rather than achieve a complete cure.
such as ‘tinnitus retraining training’ and
therapies
Masking may provide relief in conjunction: white noise (like an o- tuned radio)
ance.
is given via a noise generator worn like a post- aural hearing aid, or by enhancing background noise (eg fans).
scale trials only). If Ménière’s disease is the cause, betahistine helps only a few.
p
499
); alcohol intoxication.
459
).
pulsatile, think of
AV
fist ulae, an d glom us jugul are tu mours ).
Behavioural
CBT
can help reduce evoked annoy-
Drugs are disappointing: misoprostol appears to help (small-
Hearing loss
B
Acoustic
https://t.me/med1917
Bedside tests Whisper test Simple but sensitive: whisper numbers in one ear
while blocking the other. Make sure that failure to repeat the number is not from
misunderstanding. Failure should prompt evaluation by an audiologist.
(Rinne: bone conduction via the mastoid is louder than air conduction in con-
tests
ductive losses >
20
D
, and Weber: with the fork on the vertex, sound localizes to the
aected ear with conductive loss, to the contralateral ear in sensorineural hearing
loss, and to the midline if both ears are normal.) Designed for unilateral conductive
losses and have poor sensitivity; these should not be used as screening tests.
Conductive deafness Causes Wax (remove, eg by syringing with warm water after
softening with olive oil drops), otosclerosis, cholesteatoma, otitis media (
Chronic sensorineural deafness Often due to accumulated noise exposure,
presbycusis, or inherited disorders.
for high- frequency sounds starts before
Presbycusis Symmetrical reduction of acuity
30
yrs old. We do not usually notice it until
hearing of speech is aected. Hearing is most aected in the presence of background noise. Hearing aids are the usual treatment.
Sudden sensorineural deafness Get an
(most cases); noise exposure; gentamicin/ other toxin; mumps; acoustic neuroma;
stroke; vasculitis;
tests for
TB
’, p
TB
. Te st s
390
); audiometry;
ESR, FBC, LFT
MRI.
ENT
opinion today. Causes Idiopathic
, p
ANCA
, viral titres, and
Management All patients typically receive ster-
oids, but there is no good evidence. Antivirals are no longer recommended.
Acoustic neuroma (figs
10.13
) Doubly misnamed: it is a
Schwannoma (not neuroma)
10.12
,
Vestibular
nerve
arising from the vestibular (not
auditory) nerve. They account for
80
% of cerebellopontine angle tumours and often present with unilateral hearing loss/ tinnitus, with
vertigo occurring later. Growth
rate is slow (usually
and can be predicted by serial
MRI
S. With progression, ipsilat-
V
th, VIth, IXth, and Xth nerves
eral
may be aected (also ipsilateral
cerebellar signs). Signs of
occur late, indicating a large tumour. Commoner in and neurofibromatosis (esp.
1– 2
NF2
mm/ year)
, p
510
).
ICP
Fig 10.
12
An acoustic neuroma (vestibular Schwan-
noma) growing dangerously near the facial nerve.
TB (
see
neuroma
Tuning fork
OHCS
p
394
BOX
‘Diagnostic
2
Cochlear
nerve
Facial
nerve
).
MS
459
10 Neurology
;
(a)
Fig 10.
13
Large vestibular Schwannoma: axial T2W (a) and contrast- enhanced coronal MRI (b).
Repro duced from Manji et al., Oxford Handbook of Neurology,
University Press.
(b)
2007
with permission from Oxford
10 Neurology
Functional neurological disorders
https://t.me/med1917
460
Unexplained changes in nervous system function without structural abnormalities
make up at least a third of all outpatient neurological presentations, and are one
of the biggest causes of disability. : ≥
examination does not rule out organic pathology, ‘functional overlay’ is common.
Presentation and diagnostic signs
Fun ctio nal weak nes s
eral and possibly more common on the non- dominant side. Typically increases with
attention and decreases with distraction. Positive signs include obvious incongruence
with functional ability (eg can stand on tip toes but no ankle plantar flexion on examination), collapsing or ‘give- way’ weakness (not specific, can occur in joint problems
or pain), drift without pronation of a weak arm, Hoover’s sign (see
floodgates’) in a weak leg.
Functional sensory disturbances Sensory loss of one of more modalities is most
common. Positive signs include precise midline splitting (eg of vibration sense
across the forehead), inconsistent deficits when hand sensation is tested with the
fingers interlocked behind the back, tubular visual field defects (tunnel vision of
the same width regardless of distance, incompatible with the laws of physics), reported inaudible tuning fork test at the ipsilateral mastoid process for a reported
unilateral hearing loss (transcranial attenuation of vibration is minimal so this
should be perceived by the contralateral cochlea).
Functional gait disorders Commonly leg dragging, knee- buckling, excessive slow-
ness, or bizarre gait not conforming to a usual pattern. A useful clue is the highly
specific ‘hung and pung’ sign (excessive demonstration of eort).
Functional movement disorders Tremor is most common, and is typically variable,
distractible, and associated with isometric contraction of antagonistic muscles in
the limb. Functional myoclonus is also variable and distractible, with a predominantly axial location. Fixed dystonia at onset, and dystonia after peripheral trauma
are likely to be functional in most cases.
Psychogenic non- epileptic seizures Suspect if seizures have a gradual onset, pro-
longed duration, and abrupt termination and are accompanied by closed eyes ±
resistance to eye opening, rapid breathing, fluctuating motor activity, and episodes
of motionless unresponsiveness.
exist with true epilepsy.
Pathophysiology
‘Conversion disorder’ (psychological distress manifest in physical symptoms) is likely
only to be a part of the cause, deficient inhibition and attentional dysregulation are
also implicated. Functional
Diagnosis
Make a positive diagnosis based on suggestive signs as well as negative investigations. The delivery of the diagnosis is key; acknowledge that these are genuine
symptoms, regardless of their incongruence with known neurological disease, cause
distress and disability, and that they are potentially reversible with treatment.
Dierential diagnosis
Any neurological disorder with an atypical presentation, psychiatric disorders,
including somatic symptom disorder, depersonalization/ derealization disorder,
factious disorder (deliberately feigned to obtain care), Münchausen’s (
malingering (deliberately feigned for external benefit, eg medicolegal context).
Management
Avoid treatments directed at the symptomatology. The diagnosis alone with a
follow- up visit to rediscuss can be therapeutic. Referral to psychiatry and cognitive
behavioural therapy might be required for patients not showing signs of improvement, as well as identification and treatment of any comorbid psychiatric disorder.
History of leg dragging or dropping things, frequently unilat-
MRI
shows contrasting findings to feigned symptoms.
CNS
exam, CT,
3:1
. The presence of functional signs on
MRI
, and
EEG
are normal. It may co-
BOX
‘Opening the
p
694
), and
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