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Delirium vs dementia
https://t.me/med1917
One is often mistaken for the other, yet perhaps the interconnectedness of these
two conditions is greater than we realize: not only is dementia the leading risk
factor for delirium, but delirium itself confers a greater risk of subsequently developing dementia.
marker of vulnerability of the brain, and may also emphasize previously unrecognized dementia symptoms. Furthermore, there may be direct causation through
the noxious insults incurred during an episode of delirium, which can lead to permanent neuronal damage.
In distinguishing the two conditions (not always an easy task), the presence
of inattention, distractibility, and disorganized thinking will all point you towards
delirium. But the fundamental question is ‘Has there been an acute change from
the patient’s cognitive baseline?’ Family or carer collateral reports are invaluable, but may not always be available. Document cognition in all patients >
admitted to hospital (eg
This will then allow you to compare thei r admission score with subsequent assessments and track any improvements, deteriorations, or fluctuations in cognition throughout the admission.
9 It is likely that this is due to a number of factors: delirium is a
65
AMT
s, p61, many admission proformas allow for this).
yrs
481
10 Neurology
10 Neurology
Dementia
https://t.me/med1917
482
A neurodegenerative syndrome with progressive decline in several cognitive domains. The initial presentation is usually of memory loss over months or years (
for other causes if over days/ weeks). Prevalence increases with age:
80
yrs are known to have dementia, yet probably only half of cases are diagnosed.
>
Diagnosis Is made by: History from the patient with a thorough collateral
narrative— ask about the timeline of decline and the domains aected. Noncognitive symptoms such as agitation, aggression, or apathy indicate late disease.
Cognitive testing: use a validated dementia screen such as the
plus short tests of executive function and language. Carry out a mental state examination to identify anxiety, depression, or hallucinations.
physical cause, risk factors (eg for vascular dementia), or parkinsonism.
is important to exclude drug- induced cognitive impairment.
review
Investigations Look for reversible/ organic causes:
p
330
normals,
cose. An
haematoma,
), thiamine (eg alcohol), Ca
MRI
(preferred to CT) can identify other reversible pathologies (eg subdural
p
476
; normal- pressure hydrocephalus10), as well as underlying vascular
2
+
. Check
damage or structural pathology. Functional imaging (
lineate subtypes where diagnosis is not clear. Consider
frontotemporal dementia,
check autoantibodies, syphilis,
Subtypes • Alzheimer’s disease (AD) See p
CJD
, or a seizure disorder. If clinically indicated then
HIV, CJD
, or other rare causes (see later in topic).
484
. • Vascu lar deme ntia (~25%.)
AMTS
Examination may identify a
TSH
/
B
/ folate (treat low-
12
MSU, FBC, ESR, U&E, LFT,
FDG, PET, SPECT
EEG
in: suspected delirium,
Cumulative eect of many small strokes: sudden onset and stepwise deterioration
is characteristic (but often hard to recognize). Look for evidence of arteriopathy
BP
, past strokes, focal
(
memantine in these patients.
CNS
signs). Do not use acetylcholinesterase inhibitors or
• Lewy body dementia (15– 25%.) Fluctuating cog-
nitive impairment, detailed visual hallucinations, and later, parkinsonism (
Histology is characterized by Lewy bodies (eosinophilic intracytoplasmic inclusion
bodies) in brainstem and neocortex.
mentia (risk of
atrophy with loss of >
SE,
see p
70
% of spindle neurons. Patients display executive impair-
Avoid using antipsychotics in Lewy body de-
485
). • Fro nto tem por al dementia Frontal and temporal
ment; behavioural/ personality change; disinhibition; hyperorality; stereotyped behaviour; and emotional unconcern. Episodic memory and spatial orientation are
preserved until later stages. Pick’s disease refers to the few frontotemporal dementia patients who have Pick inclusion bodies on histology (spherical clusters of
tau- laden neurons).
Other causes Alcohol/ drug abuse; repeated head trauma; pellagra (p
Whipple’s disease (
cryptococcosis (
p
); Huntington’s (p
404
); familial autosomal dominant Alzheimer’s;
464
);
CJD (BOX
); Parkinson’s (p
CADASIL
p
263
Management Refer suspected or diagnosed dementia to integrated memory
services for further assessment and management.
that impair cognition (eg neuroleptics, sedatives, tricyclics).
interventions
Non- cognitive symptoms (eg agitation) may respond to measures
Medication (p
Non- pharmacological
such as aromatherapy, multisensory stimulation, massage, music, and animalassisted therapy.
Other considerations • Depression Common. Try an
OD
) or, if severe, mirtazapine (15– 45mg at night if e
SSRI
(eg citalopram 10– 20mg
GFR
>40). Cognitive behavioural
therapy can help with social withdrawal and catastrophic thinking.
the patient make decisions regarding medical or financial aairs? Wherever possible, allow them to. Suggest making an advanced directive or appointing a Lasting
Power of Attorney in the early stages of the disease.
20
% of people
(p61) or similar,
Medication
and glu-
) may help de-
p
490
);
(p
466
485
). Avoid drugs
• Capacity Can
look
490
240
HIV
).
).
),
;
10
Dilated ventricles without enlarged sulci. Signs: gait apraxia, incontinence, dementia;
CSF
shunts help.
Creutzfeldt– Jakob disease (
https://t.me/med1917
CJD
)
The cause is a pr ion (PrPSc), a misfolded form of a normal protein (PrPc), that can
PrPS
;
235
c leads
cases
CJD
.
transform other proteins into prion proteins (hence its infectivity).
to spongiform changes (tiny cavities ± tubulovesicular structures) in the brain.
Most cases are
worldwide) is transmitted via contaminated
form encephalopathy.
syndrome,
‘normal’ p rotein is too unsta ble, readily t ransforming to
Contaminated surgical instruments, corneal transplants, growth hormone from
human pituitaries, and blood (
CJD
should be considered in all patients presenting with rapidly progressive de-
mentia, especially if accompanied by myoclonus (present in
signs (diplopia, supranuclear palsies, complex visual disturbances, homonymous
field defects, hallucinations, cortical blindness).
complexes);
tein),
sporadic (incidence: 1– 3/ million/ yr). Varian t
CNS
tissue aected by bovine spongi-
CJD (VCJD
Inherited forms (eg Gerstmann– Sträussler– Scheinker
P102L
mutation in
CSF
markers (
MRI
. Trea tm en t N one p roven . Dea th oc curs in ~6 month s in s pora dic
PRNP
gene with ataxia ± self- mutilation), the
VCJD
only). Prion protein resists sterilization. Signs
PrPS
c. Iatrogenic causes
95
Te st s
MRI; EEG
RT- QUIC
is 92% sensitive and
(periodic sharp wave
100
% specific,10 14- 3- 3 pro-
%), depression, eye
Who will care for the carers?
Our ageing population and improvements in medicine mean that we not only have
UK
an increasing number of people with dementia in the
, but that those people are
living longer with the disease in more advanced stages. Their needs become more
complex and they become increasingly dependent. Currently, informal (mostly
family) carers of people with dementia save the
not an easy task: most dementia suerers display behavioural or psychological
UK
£11 billion a year. Yet this is
symptoms, which can be particularly distressing for the carer. Carer stress is inevitable and causes morbidity and mortality. Ameliorate this with:
• A care coordinator (via Social Services or the local Old Age Community Mental
Healthcare Team); vital to coordinate the various teams and services available:
• Laundry services for soiled linen. • Attendance allowance.
• Car badge giving priority parking. • Respite care in hospital.
• Help from occupational therapist, district
nurses, and community psychiatric nurses.
• Day services can be invaluable for stimulating patients and providing regular,
much- needed breaks for carers.
• Moral support: support groups, telephone helplines, and charities can all ease
the burden, eg
• Combatting challenging behaviour: first rule out pain, infection, and depression.
Then consider trazod one (
Haloperidol (
UK
Alzheimer’s Disease Society.
50– 300
0.5– 4
mg) can be useful in the short term.
mg at night) or lorazepam (0.5– 1mg/ 12– 24h PO).
• Council tax rebate (forms
from local council oce).
483
10 Neurology
10 Neurology
Alzheimer’s disease (AD)
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484
This leading cause of dementia is the big neuropsychiatric disorder of our times,
dominating the care of the elderly and the lives of their families who give up work,
friends, and ways of life to support relatives through the long final years as they
exit into their ‘worlds of preoccupied emptiness’. Suspect
with persistent,
11
progressive, and global cognitive impairment: visuospatial skill,
AD
in adults >40yrs
memory, verbal abilities, and executive function (planning) are all aected, unlike other dementias which may aect certain domains but not others (identify
which with neuropsychometric tests). There is also anosognosia— a lack of insight
into the problems engendered by the disease, eg missed appointments, misunderstood conversations or plots of films, and mishandling of money. Later there may
be irritability; mood disturbance (depression or euphoria); behavioural change (eg
aggression, wandering, disinhibition); psychosis (hallucinations or delusions); agnosia (may not recognize self in the mirror). There is no standard natural history.
Cognitive impairment is progressive, but non- cognitive symptoms may come and
go over months. Eventually many patients become sedentary, taking little interest
in anything.
Cause Environmental and genetic factors both play a role. Accumulation of -
amyloid peptide, a degradation product of amyloid precursor protein, results
in progressive neuronal damage, neurofibrillary tangles, numbers of amyloid
plaques, and loss of the neurotransmitter acetylcholine (
selective— the hippocampus, amygdala, temporal neocortex, and subcortical nuclei
are most vulnerable. Vascular eects are also important—
evidence of vascular dementia.
fig
10.26
95
% of AD patients show
Risk factors 1st- degree relative with AD; Down’s syndrome (in which AD is inevit-
40
able, often <
CLU
variants; vascular risk factors (BP, diabetes, dyslipidaemia, homocysteine, AF);
yrs); homozygosity for apolipoprotein E (
physical/ cognitive activity; depression; loneliness (risk ≈
APOE) E4
allele;
2
; simply living alone is
not a risk factor); smoking.
Management See p
482
for a general approach to management in dementia.
• Refer to a specialist memory service. • Acetylcholinesterase inhibitors (see
‘Pharmacological treatment’).
extra risk halves with
Prevention in the context of
25
yrs before onset of unequivocal symptoms (
~
15
yrs before
USY
USY
USY. CSF
. Cerebral hypometabolism and impaired episodic memory occur 10yrs before
. Global cognitive impairment occurs 5yrs before
• BP control (in heart failure there is a 2≈ risk of
BP
control).
AD’S
time course Changes in
USY
CSF
- amyloid are seen
) and its deposition is detected
tau protein and brain atrophy are also detected 15yrs before
USY
. Prevention will probably
be most eective before any of this starts— though there is currently insucient
evidence to recommend any specific interventions. Ultimately, there is no simple
relationship between brain structure, neurofibrillary tangles, and function.
Prognosis Mean survival = 7yrs from
USY
.
). Neuronal loss is
PICALM, CL1 &
BOX
AD;
11
‘Enduring’ doesn’t mean unfluctuating: cognition comes and goes, allowing poetic insights, as in Iris
Murdoch’s poignant self- diagnosis: ‘I am sailing into the dark’.
Pharmacological treatment of cognitive decline
Beta amyloid plaques
Neurofibrillary tangles
https://t.me/med1917
There is overlap between Lewy body dementia, AD, and Parkinson’s disease (PD),
p
491
complicating treatment decisions: levodopa (
antipsychotic drugs worsen
Acetylcholinesterase (
are all modestly eective in treating
PD
. Rivastigmine may help all three.
ACHE
) inhibitors Donepezil, rivastigmine, and galantamine
AD
) can precipitate delusions, and
and are recommended by
NICE
, though
none should be used in mild disease and they should be discontinued if there is no
worthwhile eect on symptoms. Doses:
• Donepezil: initially 5mg PO, eg doubled after 1 mon th.
• Rivastigmine: 1.5mg/ 12h initially, to 3– 6mg/ 12h. Patches are also available.
• Galantamine: initially 4mg/ 12h, to 8– 12mg/ 12h PO.
The cholinergic eects of acetylcholinesterase inhibitors may exacerbate peptic
ECG
ulcer disease and heart block. Ask about symptoms and do an
Antiglutamatergic treatment Memantine (an
AD
ably eective in late- stage
ease or those with moderate disease in which
5
mg/ 24h initially, by 5mg/ d weekly to 10mg/ 12h. SE: hallucinations, confu-
Dose:
, and is recommended in patients with severe dis-
NMDA
antagonist, p
ACHE
inhibitors are not tolerated/ CI.
first.
445
) is reason-
sion, hypertonia, hypersexuality.
Amyloid- beta monoclonal antibodies Aducanumab (monthly IV infusion) was a
promising development that has been controversially approved by the
refused in Europe in view of weak supportive evidence in mild
US FDA,
PET-
confirmed AD.
There is more promising recent evidence for lecanemab, but both are associated
with amyloid- related imaging abnormalities (oedema or haemorrhage).
Antipsychotics Consider in severe, non- cognitive symptoms only (eg psychosis
or extreme agitation).
Possible increased risk of stroke/
assess cerebrovascular risk factors. Avoid in mild- to- moderate: Lewy body dementia (risk of neuroleptic sensitivity reactions),
TIA
so discuss risks and
AD
, and vascular dementia.
Vitamin supplementation Trials of dietary and vitamin supplements have been
E
(
mixed and disappointing. Perhaps the best evidence exists for vitamin
OD
) which may confer a modest benefit in delaying functional progression in mild-
to- moderate
AD
, but with no eect on cognitive performance.
2000IU
485
10 Neurology
but
Normal neuron
Fig 10.
26
plaques and neurofibrillary tangles (right). The corresponding changes on functional neuroimaging are also shown.
Normal neuron (left) and one exhibiting senile
10 Neurology
Epilepsy: diagnosis
OHCS
https://t.me/med1917
486
Epilepsy is a recurrent tendency to spontaneous, intermittent, abnormal electrical
activity in part of the brain, manifesting as seizures. Convulsions are the motor
signs of electrical discharges.
Elements of a seizure Some patients may experience a preceding prodrome
lasting hours or days in which there may be a change in mood or behaviour. An
aura implies a focal seizure, often, but not necessarily, from the temporal lobe. It
may be a strange feeling in the gut, an experience such as déjà vu or strange smells
or flashing lights. Post- ictally there may be headache, confusion, and myalgia; or
temporary weakness after a focal seizure in the motor cortex (Todd’s palsy,
dysphasia following a focal seizure in the temporal lobe.
Causes ⅔ are idiopathic. Structural Cortical scarring (eg head injury years be-
fore onset), developmental (eg dysembryoplastic neuroepithelial tumour or cortical
dysgenesis), space- occupying lesion, stroke, hippocampal sclerosis (eg after a febrile convulsion), vascular malformations.
SLE, PAN,
antibodies to voltage- gated potassium channels.
Others Tuberous sclerosis, sarcoidosis,
Diagnosis Can be dicult due to the heterogeneous nature of the disease (there
40
dierent types of epilepsy).
are >
have been wrongly diagnosed.
cialist assessment and investigation in <
NICE
estimate 5– 30% of people with ‘epilepsy’
All patients with a seizure must be referred for spe-
2
wks.
Take a thorough history Including a detailed description from a witness. Ask spe-
cifically about tongue- biting and a slow recovery. If this is a first seizure, enquire
about past funny turns/ odd behaviour. Déjà vu and odd episodic feelings of fear
may well be relevant. Are there any triggers (eg alcohol, stress, flickering lights/
TV)
? Triggered attacks tend to recur.
Establish the type of seizure See
chogenic non- epileptic seizures (
BOX
‘Seizure classification’. Don’t forget psy-
p
460
).
Rule out provoking causes Most people would have a seizure given sucient
provocation (eg reflex anoxic seizures in faints) but would not be classed as epileptic: only
irreversible. Causes: trauma; stroke; haemorrhage;
withdrawal; metabolic disturbance (hypoxia, Na
disease); infection (eg meningitis, encephalitis);
Unprovoked seizures have a recurrence rate of 30– 50%.
Investigations Look for provoking causes. Consider an
lepsy and can be falsely + ve, so don’t do one if simple syncope is the likely diagnosis.
Only do emergency
(structural lesions); drug levels (if on anti- epileptics: is the patient adherent?); drugs
screen;
3– 10
% of provoked seizures recur; generally when the provocation is
EEG
S if non- convulsive status is the problem. Other tests:
LP
(eg if infection suspected).
ICP
; alcohol or benzodiazepine
+
2
+
, Ca
, glucose, uraemia, liver
T
°; drugs (tricyclics, cocaine).
EEG
: it cannot exclude epi-
Counselling After any ‘fit’, advise about dangers, eg swimming, driving, heights until
the diagnosis is known; then give individualized counselling on employment, sport, insurance, and conception (
until seizure- free for >
p32). The patient must contact
1
yr, or >6mths for a one- o awake s eizure (p
DVLA
p
696
), or
MRI
and avoid driving
151
).
Seizure classification
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Focal seizures Originating within networks linked to one hemisphere and often
seen with underlying structural disease. Various subclasses include:
• Without impairment of consciousness (Previously described as ‘simple’.) Awareness
is unimpaired, with focal motor, sensory (olfactory, visual, etc.), autonomic, or psychic
symptoms. No post- ictal symptoms.
• With impairment of consciousness (Previously described as ‘complex’.) Awareness
is impaired— either at seizure onset or following a simple partial aura. Most commonly arise from the temporal lobe, in which post- ictal confusion is a feature.
• Evol ving to a bilateral, convulsive seizure (Previously described as ‘secondary
generalized’.) In ⅔ of patients with partial seizures, the electrical disturbance,
which starts focally, spreads widely, causing a generalized seizure, which is typically convulsive.
Generalized seizures Originating at some point within, and rapidly engaging
bilaterally distributed networks leading to simultaneous onset of widespread
electrical discharge with no localizing features referable to a single hemisphere.
Important subtypes include:
• Absence seizures Brief (≤10s) pauses, eg suddenly stops talking in mid- sentence,
then carries on where left o. Presents in childhood.
• To n ic – clonic seizures Loss of consciousness . Limbs stien (tonic), then jerk (clonic).
May have one without the other. Post- ictal confusion and drowsiness.
• Myoclonic seizures Sudden jerk of a limb, face, or trunk. The patient may be thrown
suddenly to the ground, or have a violently disobedient limb: one patient described it
as ‘my flying- saucer epilepsy’, as crockery which happened to be in the hand would
take o.
• Atonic (akinetic) seizures Sudden loss of muscle tone causing a fall, no
• Infantile spasms (
NB
: the classification of epileptic syndromes is separate to the classification of
seizures, and is based on seizure type, age of onset,
tures such as family history.
OHCS
p
232
) Commonly associated with tuberous sclerosis.
EEG
findings, and other fea-
LOC
.
Localizing features of focal seizures
Temporal lobe • Automatisms— complex motor phenomena with impaired
awareness, varying from primitive oral (lip smacking, chewing, swallowing)
or manual movements (fumbling, fiddling, grabbing), to complex actions.
• Dysphasia. •Déjà vu (when everything seems strangely familiar), or jamais vu
(everything seems strangely unfamiliar).
terror, panic, anger, or elation, and derealization (out- of- body experiences).
• Hallucinations of smell, taste, or sound. • Delusional behaviour. • Bizarre
associations— eg ‘Canned music at Tesco always makes me cry and then pass out’.
Frontal lobe • Motor features such as posturing or peddling movements of the
• Jacksonian march (a spreading focal motor seizure with retained aware-
legs.
ness, often starting with the face or a thumb).
ioural disturbances (often diagnosed as psychogenic).
• Post- ictal Todd’s palsy (p
arrest.
Parietal lobe • Sensory disturbances— tingling, numbness, pain (rare). • Motor
symptoms (due to spread to the pre- central gyrus).
Occipital lobe • Visual phenomena such as spots, lines, flashes.
• Emotional disturbance, eg sudden
• Motor arrest. • Subtle behav-
696
).
• Dysphasia or speech
487
10 Neurology
10 Neurology
Epilepsy: management
ASM
ASM
https://t.me/med1917
488
Living with epilepsy creates many problems: inability to drive and drug side eects
to name a few. Good management of the condition by an integrated specialized
team is therefore of utmost importance.
Anti-seizure medications (
confirmed epilepsy diagnosis, ≥
tural brain lesion, focal
a detailed discussion of treatment options with the patient.
seizure type and epilepsy syndrome, comorbidities, lifestyle, and patient preference:
• Focal (partial) seizures 1st line: carbamazepine or lamotrigine. 2nd line:
levetiracetam, oxcarbazepine, or sodium valproate.
• Generalized tonic– clonic seizures 1st line: sodium valproate12 or lamotrigine. 2nd
line: carbamazepine, clobazam, levetiracetam, or topiramate.
• Absence seizures 1st line: sodium valproate12 or ethosuximide. 2nd line:
lamotrigine.
• Myoclonic seizures 1st line: sodium valproate.12 2nd line: levetiracetam, or
topiramate (but
seizures.
• Tonic or atonic seizures Sodium valproate12 or lamotrigine.
Treat with one drug and with one doctor in charge only. Slowly build up doses
2– 3
months (see
over
trolled or maximum dosage is reached. If ineective or not tolerated, switch to the
next most appropriate drug. To switch drugs, introduce the new drug slowly, and
only withdraw the
necessary in <
s) Should only be commenced by a specialist, after
2
seizures (unless risk of recurrence is high, eg struc-
CNS
deficit, or unequivocal epileptiform
12
SE
). Avoid carbamazepine and oxcarbazepine— may worsen
BOX
‘Anti-seizure medications (
1
st drug once established on the 2nd. Dual (adjunct) therapy is
10
% of patients— consider if all appropriate drugs have been tried
ASM
EEG
choice depends on
s)’) until seizures are con-
singly at the optimum dose.
Stopping
ASM
s May be done under specialist supervision if the patient has been
2
seizure- free for >
the need to drive). The dose must be decreased slowly: over at least
6
months for benzodiazepines and barbiturates.
>
yrs and after assessing risks and benefits for the individual (eg
Other interventions Psychological therapies Eg relaxation,
some, but do not improve seizure frequency so only use as an adjunct to medication.
Surgical intervention Can be considered if a single epileptogenic focus can be iden-
tified (such as hippocampal sclerosis or a small low- grade tumour). Neurosurgical
resection oers up to
causing focal neurological deficits. Alternatives: vagal nerve stimulation, deep brain
stimulation (
DBS
Sudden unexpected death in epilepsy (
epilepsy, and may be related to nocturnal seizure- associated apnoea or asystole.
Those with epilepsy have
UK
yr in the
; up to 17% are
70
% chance of seizure resolution, but carries the risk of
).
SUDEP
) More common in uncontrolled
3
≈ mortality. >
SUDEP
700
S. The charity
epilepsy- related deaths are recorded/
SUDEP
Action may be of some help to
families.
), and following
2– 3
months, or
CBT
. May benefit
12
Sodium valproate is associated with significantly risk of birth and developmental defects in children
born to exposed mothers. The rates of congenital abnormality (neural tube defects) are
of children born are found to have a degree of non- developmental disability. Use in women of childbearing
potential with caution and only after counselling.
10
% and 30– 40%
Anti-seizure medications (
https://t.me/med1917
Carbamazepine (As slow- release.) Initially
2
wks up to max
every
paired balance, drowsiness, mild generalized erythematous rash (check pres-
HLAB1502
ence of
necrolysis),
allele in Han Chinese populations due to risk of toxic epidermal
SIADH
(rare; see p
ASM
S): typical adult doses and side eects
100
1000
mg/ 12h. SE: leucopenia, diplopia, blurred vision, im-
665
).
mg/ 12h, increase by
200
mg/ d
Lamotrigine As monotherapy, initially 25mg/ d, by 50mg/ d every 2wks up to
100
mg/ 12h (max
if on carbamazepine or phenytoin (max
occurs in
necrolysis) typically in
doctor at once if rash or flu symptoms develop; Other
10
% (but 1/
250
mg/ 12h). Halve monotherapy dose if on valproate; double
1000
develop Stevens– Johnson syndrome or toxic epidermal
1
st 8wks, especially if on valproate; warn patients to see a
350
mg/ 12h). SE: maculopapular rash—
SE
: diplopia, blurred vision,
photosensitivity, tremor, agitation, vomiting, aplastic anaemia.
Levetiracetam Initially
1.5
g/ 12h (if e
GFR
tation. Other
Sodium valproate Initially
30
mg/ kg (or 2.5g) daily. SE: teratogenic. Nausea is very common (take with food).
SE
: liver failure (watch
Other
250
mg/ 24h, increase by
250
mg/ 12h every 2wks up to max
>80). SE: psychiatric side eects are common, eg depression, agi-
SE: D&V
, dyspepsia, drowsiness, diplopia, blood dyscrasias.
300
mg/ 12h, increase by
LFT
especially during 1st 6 months), pancreatitis, hair
100
mg/ 12h every 3d up to max
loss (grows back curly), oedema, ataxia, tremor, thrombocytopenia, encephalopathy (hyperammonaemia).
Phenytoin No longer 1st line due to toxicity (nystagmus, diplopia, tremor, dys-
SE
arthria, ataxia) and
: intellect, depression, coarse facial features, acne, gum
hypertrophy, polyneuropathy, blood dyscrasias. Blood levels required for dosage.
Carbamazepine, phenytoin, and barbiturates are liver enzyme inducing.
Epilepsy and pregnancy
Epilepsy carries a 5% risk of fetal abnormalities, so good seizure control prior
to conception and during pregnancy is vital. Yet some anti- epileptics are teratogenic: the patient must be given accurate information and counselling about
contraception, conception, pregnancy, and breastfeeding in order to make informed decisions. In particular:
• Advise women of child- bearing age to take folic acid 5mg/ d.
• Strictly avoid sodium valproate and polytherapy before conception and during
pregnancy (lamotrigine is preferred but transition needs to be planned).
• Advise that most
milk. Lamotrigine is not thought to be harmful to infants.
• Discuss contraceptive methods, bearing in mind that: enzyme- inducing
progesterone- only contraception unreliable, and oestrogen- containing contracep-
ASM
S except carbamazepine and valproate are present in breast
ASM
S make
tives lower lamotrigine levels— an increased dose may be needed to achieve seizure
control.
489
10 Neurology
10 Neurology
Parkinsonism
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490
This is the extrapyramidal triad of:
1
Tremor. Worse at rest; often ‘pill- rolling’ of thumb over
fingers (see
2
Hypertonia. Rigidity + tremor gives ‘cogwheel rigidity’,
felt by the examiner during rapid pronation/ supination.
3
Bradykinesia. Slow to initiate movement; actions slow
and decrease in amplitude with repetition, eg
rate, micrographia. Gait is festinant (shuing, pitched
forward,
tacles or doors (due to poor simultaneous motor and
p
464
).
fig
10.27
) with arm- swing and freezing at obs-
blink
cognitive function). Expressionless face.
Causes Parkinson’s disease (PD) Loss of dopaminergic
neurons in the substantia nigra, associated with Lewy bodies
in the basal ganglia, brainstem, and cortex. Most cases are
sporadic, though multiple genetic loci have been identified in
familial cases. Mean age at onset is
3.5
% at 85– 89yrs. Clinical features The parkinsonian
age:
triad, plus non- motor symptoms such as: autonomic dys-
60
yrs. Prevalence with
Fig 10.
petit pas.’
function (postural hypotension, constipation, urinary frequency/ urgency, dribbling
of saliva), sleep disturbance, and reduced sense of smell. Neuropsychiatric complications, such as depression, dementia, and psychosis, are common and debilitating.
Diagnosis Is clinical and based on the core features of bradykinesia with resting
tremor and/ or hypertonia; cerebellar disease and frontotemporal dementia should
be excluded; a clinical response to dopaminergic therapy is supportive.
are invariably worse on one side— if symmetrical look for other causes. If an alternative cause is suspected then consider
Functional neuroimaging (DaTscan™,
Focuses on symptom control and does not slow disease progression (see
pharmacological options include deep brain stimulation (
MRI
to rule out structural pathology.
PET
) is playing an emerging role. Treatment
DBS
, may help those who
are partly dopamine responsive) and surgical ablation of overactive basal ganglia
circuits (eg subthalamic nuclei).
Parkinson’s plus syndromes Progressive supranuclear palsy (
Richardson– Olszewski syndrome.) Early postural instability, vertical gaze palsy ±
falls; rigidity of trunk > limbs; symmetrical onset; speech and swallowing problems; little tremor.
features, eg impotence/ incontinence, postural
gidity > tremor.
limb; cortical sensory loss (eg astereognosis); apraxia (even autonomous interfering
activity by aected limb— the ‘alien limb’ phenomenon).
See p
482
.
Multiple system atrophy (
Cortico- basal degeneration (
MSA
; Shy– Drager.) Early autonomic
BP
; cerebellar + pyramidal signs; ri-
CBD
.) Akinetic rigidity involving one
Lewy body dementia
Secondary causes Vascular parkinsonism (2.5– 5% of parkinsonism, also called
‘lower limb’ parkinsonism). Eg diabetic/ hypertensive patient with postural instability and falls (rather than tremor, bradykinesia, and festination).
ondary causes
toxins (manganese), Wilson’s disease (
alitis, neurosyphilis
Management Requires input of a multidisciplinary team (
Drugs (neuroleptics, metoclopramide, prochlorperazine, valproate),
p
281
.
), trauma (dementia pugilistica), enceph-
GP,
neurologist, nurse specialist, social worker, carers, physio- and occupational therapist) to boost quality of
life. Assess disability and cognition objectively and regularly, and monitor mood—
depression is common. Involve palliative care services early on. Postural exercises
and weight lifting may help.
Don’t forget the carers (p
483
): oer respite care.
27
‘Marche à
Signs
BOX
). Non-
PSP
, Steele–
Other sec-
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