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Neurology Drugs
Neurology Drugs
NAME Mechanism of Effects Dosage Side effects Indication Contraindication Core Adverse
action drug reactions/notes/
or not interactions
L-dopa/DOPA It is combine with Oral and SC Acute side effects This is the contraindicated core The therapeautic
decarboxylase a peripherally modified or include: first line in patients with effect decreases as
inhibitor acting dopa slow release Nausea and anorexia – treatment for narrow angle the disease advances
combinations decarboxylase preparations domperidone PD glaucoma or as part of its action
Such as sinemet inhibitor such as have been (dopamine antagonist psychotic illness rely on the presence
(combination of carbidopa or developed that workings CTZ can It overall and should be of functional
carbidopa and benserazide prevent) increases the avoided dopaminergic
levodopa) To reduce Postural hypotension life in patients neurones
peripheral side Hallucinations and expectancy of receiving
effects delusions PD patients monoamine In patients troubled
Confusion probably as a oxidase type A with end of dose
It replaces Insomnia result of (MAO-A) motor fluctuations, a
dopamine Nightmares motor inhibitors. triple combination
Decarboxylation disorientation function of entacapone,
occurs rapidly although carbidopa and
within the brain There are two main some levodopa is used
because the types of unwanted symptoms
decarboxylase effects: such as
inhibitors i.e. dysphagia,
carbidopa do not Involuntary cognitive
cross the BBB movements decline are
not improved
Tardive Dyskinesia –
these do not develop
initially but develop in
majority of patients
within 2 years of
starting therapy.
Movements usually
affect the face and
limbs and can be
severe. They occur at
time of peak
therapeautic effect
Levodopa is short
acting and the
fluctuating plasma
concentration of the
drug may favour the
development of
dyskinesias, as longer-
acting dopamine
agonists are less
problematic in this
regard.
Rapid fluctuations in
clinical state
where bradykinesia
and rigidity may
suddenly worsen for
anything from a few
minutes to a few
hours, and then
improve again. This
‘on–off effect’ is not
seen in untreated PD
patients or with other
anti-PD drugs. As with
the dyskinesias, the
problem seems to
reflect the fluctuating
plasma concentration
of levodopa
Dopamine These act directly They have a SE of ergot derived: Less efficacy core Ergot derived:
agonist on striatal short than L-dopa There is a risk of
ergot derived: dopamine plasma life Postural hypotension but less risk of fibrotic reactions in
Apomorphine- receptors. They (6-8) which Hallucination motor the lungs,
non-oral, exhibit a slight means they Sedation complications retroperitoneum and
pergolide, selectivity for D2 require TDS Nausea and vomiting One of the pericardium
carbegoline over D1 dosage three first line
though slow Apormorphine can in early
non-ergot release lead to mood and disease
derived: formations behavioural changes, Apomorphine
ropenirole, are now cardia dysrhythmias, is sometimes
rotigotine available hypotension and is a used to
last resort if other control the
drugs fail on-off effect
of levodopa
Non ergot derived: however it
Better tolerated and must be
do not show combined
fluctuations with an oral
Somnolence anti-emetic
Fatigue because of its
Peripheral oedema antiemetic
Confusions actions
Orthostatic
hypotension
Hallucinations
May predispose to
compulsive behaviours
topiramate
metoclopramide
ondasetron
cyclizine
Carbamazepine Sodium channel It is chemically related to Treatment rash; It is effective It is a strong Core
inhibitor. It acts TCAs should start dose related in most forms inducer of liver
by use-dependent It can act as an at a low drowsiness, of seizures enzymes and so
antagonism (that antiepileptic dose which ataxia, except can accelerate
is it blocks the Useful for neuropathic pain is usually water retention; absence the metabolism
most hyperactive Useful as an anti-manic built up diplopia or blurred seizures. of other drugs
cells and the drug gradually to vision It is also such as
higher the avoid dose- hyponatraemia; useful in warfarin,
frequency of related thrombocytopeni or neuropathic phenytoin, oral
activation, the toxicty leukopenia (especially pain such as contraceptives
greater the block in people of Asian trigeminal and
produced). This origin) neuralgia corticosteroids
characteristic, can cause more severe It can be used
which is relevant mental and motor for focal
to the ability of disturbances seizures
drugs to block the incidence and severity Especially
high-frequency of side effects are useful in
discharge that relatively low temporal
occurs in an compared to other lobe epilepsy
epileptic fit drugs can be used
without unduly for trigeminal
interfering with neuralgia
the low-frequency
firing of neurons
in the normal
state
Sodium Sodium and It also causes a significant abdominal pain or It is first line It is teratogenic, Core
valproate calcium channel increase in the GABA nausea, hair loss or for men in causing spina
blocker. It is a content of the brain. It can curling in about 10% of generalised bifida and other
simple cause thinning of hair in seizures neural effects
patients, weight gain,
monocarboxylic about 10% of patients and Can be used
acid which is may cause hepatitis. tremor, for absence
chemically thrombocytopenia seizures
unrelated to any most serious side
other class of AED effect is hepatotoxicity
Status
epilepticus
pre-hospital
topimarate Appears to do a Clinical efficacy is similar to drowsiness, weight Used mainly
little of phenytoin and it produces loss, renal stones, as an add on
everything, less side effects paraesthesiae. therapy in
blocking sodium refractory
and calcium cases of
channels and partial and
enhancing the generalisd
action of GABA siezures
magnesium Magnesium also
competes with
calcium in voltage
gated calcium
channels (NMDA)
and so an increase
in the
concentration of
magnesium will
inhibit
transmission.