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41 Cards in this Set
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- Back
With regards to extrapyramidal movement disorders |
They may be reversible on ceasing antipsychotics They are less with conventional antipsychotics compared with atypical antipsychotics Dystonic reactions more commonly affect muscles of the back and arms Parkinsonism occurs late (after years) in the Rx with anti psychotics Akathisia is involving muscles of face and neck
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What is the basis of developing EPSE |
Extrapyramidal function refers to our motor control and coordination, including being able to not make movements we don't want to make. Extrapyramidal side effects from medications are serious. EPSEs are largely consequent upon post-synaptic dopamine blockade in the extrapyramidal system: those core evolutionarily archaic parts of the brain that enable us to maintain posture and tone, the basic building blocks of movement. |
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What are the features of Parkinsonism |
Rigidity Tremor Restriction of affect
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What are the main forms of EP movement disorders |
1.Parkinsonism 2.Dystonias 3.Dyskinesias 4.Akathisia
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What are the key features of Parkinsonism rigidity |
The individual experiences a rigidity of the joints, with a characteristic ‘cog-wheeling’ evident throughout the range of passive movement: |
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What is the type of rigidity seen in contralateral cortical insult (stroke) |
the ‘clasp-knife’ rigidity |
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What clinical features are seen as a result of rigidity |
The rigidity makes movements slow and shuffling gait and inability to negotiate a three-point turn are characteristic features.Lack of arm swing while walking is an early sign, demonstrated by asking the individual to extend their arms laterally and drop them to their sides. Normal tone allows a rapid fall with a characteristic ‘double slap’ that disappears early in the course of Parkinsonism. |
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How long does it take for them to develop |
These can all occur early (within hours, days or weeks of exposure to an antipsychotic medication), but can also have a delayed onset (years), notably in tardive dyskinesia, thought to be due to up-regulation of the dopamine system after chronic blockade. |
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What are the features of Parkinsonism tremor |
There is a characteristic form of tremor associated with Parkinsonism: a slow (4-6Hz) movement of the thumb across the other fingers, a movement which has earned the descriptor ‘pill-rolling’ tremor. Some people with Parkinsonism also experience other tremors, notably a fine resting tremor but this is a very non-specific type of movement disorder . It can be brought out by placing a sheet of paper on the individual’s outstretched hands. |
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What are the features of restriction to affect |
the individual manifest little by way of facial expression even if the topic being discussed is emotionally charged. |
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How do you assess them |
•Ask the patient to walk to the door and then turn around and walk back: note in particular any reduction in the fluidity of gait, shuffling and difficulty performing a three-point turn; and reduced arm swing and a tendency for the arms to move in synchrony with the legs. In more severe cases festination might be apparent. Observe also for the classic ‘pill-rolling’ tremor.•Ask the patient to hold their arms out to the side and let them fall with gravity to their sides: observe the rapidity to arm drop and the normal ‘double slap’ against the thighs.•Explain to the patient that you want to feel the tone in their wrists and elbows and ask them to relax and neither to resist not assist you. The joints should be moved slowly, then ask the patient to move their head from side to side, as this can bring out latent cog-wheel rigidity. Ensure you perform this exercise on both left and right as rigidity can be asymmetrical.•Observe the patient’s range of facial expression, notably whether there is variation. Try to put the patients at ease as affect can be restricted in the person is anxious or depressed. It can be useful to perform a glabellar tap, a positive sign being a failure to habituate (ie. stop blinking) to a light but firm taps to the forehead
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What are atypical antipsychotics |
Newer medications
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Which medications have more chances of giving rise to EPSE |
Older ones-typical But can and do occur with any type of antipsychotic. Antidepressants and other medications can sometimes cause extrapyramidal side effects as well. |
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Y |
Of course, this is vastly simplistic as a number of the older (‘first generation’) drugs have inherent anticholinergic properties, e.g. chlorpromazine) that make them less likely than the purer dopamine D2 blockers such as haloperidol, to result in Parkinsonism.Also, some of the atypical agents such as risperidone, paliperidone and amisulpride tend, at higher doses, to emulate their historically older cousins in terms of EPSE induction.
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Y |
The advent of the newer so-called ‘atypical’ antipsychotics has meant that prescribers have a wide range of agents from which to choose; and generally, the newer medications have a lower propensity than the older ones, to cause EPSE.But certainly, should a patient experience Parkinsonism on a certain medication, the first option would be to try to switch the drug to one with a lower risk thereof. Should that manoeuvre fail or be otherwise contraindicated, the addition of regular anticholinergic treatment could be employed: 1-2mg of benztropine usually suffices, albeit some patients require higher doses.
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What are the causes of tremor that can be seen in Parkinsonism as well |
anxiety, familial essential tremor, thyrotoxicosis, alcohol withdrawal and treatment with lithium. |
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What is dystonia |
Dystonia refers to an abnormality of tone, such that increased motor tone results in a sustained abnormal posture. Most striking is the acute variant, which can be frightening, painful and even fatal (e.g. laryngeal dystonia). At its most extreme, the individual exhibits severe spasm of the muscles, with the strongest muscles prevailing: thus the back arches, the limbs extend, the head is pulled back, and the tongue protrudes; the eyes also roll back in the head.
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Which muscle groups are commonly affected in dystonia |
St |
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When can it be dramatic |
There is no mistaking this emphatic clinical picture, which can occur shortly after exposure to a dopamine antagonist. |
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When can it get mixed up |
But less dramatic forms can be missed and tardive forms can be mistaken for other problems: for example, a limp might be interpreted as due to a leg problem when it is a manifestation of chronic paraspinal muscle spasm. |
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How can you treat acute dystonia |
Immediate treatment entails reassurance of the patient, ensuring they are breathing freely, and administering an anticholinergic agent such as benztropine (2mg) orally, intramuscularly or – in extreme cases – intravenously. Relief is usually dramatic.
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How do you manage chronic dystonia |
consider changing the offending medication or at least reducing the dose: if these strategies are not clinically sensible, longer-term use of an anticholinergic agent can be employed, albeit there is some evidence to suggest this increases the risk of tardive dyskinesia. |
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Examples of dystonic movements |
cervical dystonia with retrocollis and torticollis to the left, jaw-opening dystonia, blepharospasm, truncal dystonia with opisthotonic trunk posturing, proximal arms dystonia with arm extension and internal rotation, and proximal legs dystonia. |
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What is dystonia |
which is when your muscles involuntarily contract and contort. This can lead to painful positions or movements |
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What is Akathisia |
which is a feeling of restlessness, making it hard to sit down or hold still. Symptoms include tapping your fingers, rocking, and crossing and uncrossing your legs. (an inner restlessness such that the individual feels ‘compelled’ to move but movement actually does little to alleviate it, leading to overt and relentless movement of the legs in particular) |
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What is the condition quite similar to Akathisia |
Restless leg syndrome |
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What is the difference between the two |
unlike restless leg syndrome , which occurs mostly at night, akathisia is experienced right through the day: it can be particularly frustrating at night, as the compulsion to move is difficult to accommodate, and it can lead to insomnia. |
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What are the two components of akathisia |
objective restlessness (which in itself can be mistaken for anxiety, or psychotic agitation)
subjective feeling described above: one patient described it as ‘an itch deep in my very bones |
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What causes akathisia |
No antipsychotic – clozapine possibly again being the exception – is free from akathisic potential. Whilst the newer agents have a relatively lower propensity than the older ones, to induce severe akathisia, the dopamine partial agonists, due to their inherent dopamine agonism, are particular culprits, albeit brexpiprazole has a much lesser effect than aripiprazole, due to the former having lower dopamine agonism. |
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Why should we treat akathisia |
Akathisia can be enormously unpleasant and has even been associated with suicidality.It needs to be recognised and treated in a targeted manner and not dismissed as psychotic agitation:
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How do we treat akathisia |
Reduce the dose of the antipsychotic If lower dosing is not feasible or is ineffective, various agents might be useful in the shorter term to reduce akathisia.These include beta-blockers (beware of asthma and lowing of blood pressure) benzodiazepines (beware of dependence) and the antidepressant mirtazapine, which has the added virtue of hypnotic effects (beware longer-term weight gain).
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What is dyskinesia |
which is when you have uncontrollable facial movements such as sucking or chewing, lip smacking, sticking your tongue out or blinking your eyes repeatedly. |
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Which type of dyskinesia is seen in EP movement disorders |
TARDIVE - which means late onset |
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What are the clinical manifestations of tardive dyskinesia |
The main focus is on the mouth and lips, and it can begin with subtle lip movements such as repeated pursing of the lips; as it evolves the tongue can become involved, with licking movements and more noticeable lip smacking. In its full form, it is quite unmissable, with repeated unsightly oro-facio-bucco-lingual movements that can make swallowing difficult. The trunk and limbs can also be involved, but usually to a lesser degree.
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What are the risk factors for tardive dyskinesia |
long-term exposure to antipsychotic agents (especially at high dose): the first generation drugs seem to carry a higher risk than those from the second generation.Older age, greater illness severity and being female have also been cited as risk factors for tardive dyskinesia, but these may be confounded and teasing all the factors apart is difficult.
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What is the pathogenesis of tardive dyskinesia |
T |
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What is tardive dyskinesia. . |
Tardive dyskinesia is thought to be due to hypersensitivity (supersensitivity) of the dopamine system, hence merely adding anticholinergic drugs is usually of no benefit.Indeed, stopping the offending antipsychotic is also no solution: the movement disorder can become even more pronounced.Of the antipsychotics, clozapine is both least likely to cause tardive dyskinesia, as well as sometimes ameliorating the symptoms.
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What are symptoms |
Treatment of these symptoms depends upon the medication that induced them and which symptoms you have. Your doctor may try decreasing your dose or switching your medication altogether to one that has been shown to have fewer extrapyramidal side effects. |
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Why do antipsychotics cause EPSE |
I |