Integrative Flashcards
What is the difference between speech and language?
speech = how we say sounds and words
language = the words we use and how we use them
How can communication be improved wiht patients who have speech and language difficulties?
use simple language one topic at a time give more time use gesture, drawing, writing use adult language write down key words closed questions don't pretend to understand
Define dysarthria
speech disorder caused by disturbance of muscular control.
Define dysphasia
impaired ability to understand or use the spoken word.
It is due to a lesion of the dominant hemisphere and may include impaired ability to read, write and use gestures.
Define receptive dysphasia
difficulty in comprehension,
language that is fluent with a normal rhythm and articulation but it is meaningless
they fail to comprehend what they are saying.
Define expressive dysphasia
difficulty in putting words together to make meaning
not fluent and have difficulty forming words and sentences.
There are grammatical errors and difficulty finding the right word.
In severe cases they do not speak spontaneously but they usually understand what is said to them.
What is meant by the term dominant hemisphere and what is its clinical significance
The speech area is in the left, dominant side of the brain in about 99% of right-handed people.
In left-handed people, the right hemisphere is the dominant side in only 30%.
As a general rule, a lesion of the left hemisphere will cause dysphasia
What deficits will a lesion in the non dominant hemisphere cause
neglect, visuo-spatial and cognitive problems.
define dyspraxia
partial loss of the ability to co-ordinate and perform skilled, purposeful movements and gestures with normal accuracy
can affect:
Gross and fine motor skills.
Motor planning and the organisation of movement
Speech and language
Ability to carry out activities of daily living.
At what age does idiopathic parkinson’s disease most commonly start
between the ages of 55 and 65 years
What causes idiopathic PD
progressive neurodegenerative condition resulting from the death of dopaminergic neurones of the nigrostriatal pathyway.
This pathway goes from the pars compacta of the substantia nigra to the striatum. It acts to stimulate the cerebral cortex to initate movement and fine tune movement.
Therefore, when this pathway degenerates there are problems in initiating movement and fine tuning movement.
What are the key characteristics of PD
tremor
rigidity
bradykinesia
Describe the tremor in PD
Pill rolling – thumb over fingers
4-6 cycles/second
Worse at rest
Describe the rigidity of PD
increase in resistance to passive movement that can produce a characteristic flexed posture in many patients.
Cogwheel
Describe the bradykinesia in PD
Slow to initiate movement Slow, low amplitude repetitive actions eg. Blinking, micrographia, monotonous speech Gait! - Decreased arm swing - Festinance - Freezing at obstacles and doors Expressionless face
What is festinance
- Shuffling gait with flexed trunk
Give some other symptoms associated with PD
- Depression
- Dementia
- Poor decoding of emotional content of speech
- Poor executive functioning
- Visual hallucinations
- Reduced sense of smell
- Dribbling of saliva
- Frequency/urgency
- Constipation
Give the key characteristics of the gait in PD
- Reduced stride length - shuffling
- Hesitancy - difficulty starting and turning
- Lack of arm swing
- Unsteadiness – tendency to fall forwards or backwards
- Freezing at obstacles and doors
How many steps are there in the diagnostic criteria for PD
three
What is step 1 in diagnosis of PD
Bradykinesia (slowness of initiation of voluntary movement with progressive reduction in speed and amplitude or repetitive actions)
and at least one of the following:
• Muscular rigidity.
• 4- to 6-Hz resting tremor.
• Postural instability not caused by primary visual, vestibular, cerebellar or proprioceptive dysfunction.
What is step 2 in diagnosis of PD
exclusion criteria:
- History of repeated strokes with stepwise progression of Parkinsonian features.
- History of repeated head injury.
- History of definite encephalitis.
- Oculogyric crises. = dystonic reaction to certain drugs or medical conditions characterized by a prolonged involuntary upward deviation of the eyes
- Neuroleptic treatment at onset of symptoms.
- More than one affected relative.
- Sustained remission.
- Strictly unilateral features after three years.
- Supranuclear gaze palsy.
- Cerebellar signs.
- Early severe autonomic involvement.
- Early severe dementia with disturbances of memory, language and praxis.
- Babinski’s sign.
- Presence of a cerebral tumour or communicating hydrocephalus on CT scan.
- Negative response to large doses of L-dopa (if malabsorption excluded).
- Exposure to MPTP.
What is step 3 of diagnosis of PD
supportive prospective criteria. need 3 or more for diagnosis of PD
- Unilateral onset.
- Rest tremor present.
- Progressive disorder.
- Persistent asymmetry affecting the side of onset most.
- Excellent response (70-100%) to L-dopa.
- Severe L-dopa-induced chorea.
- L-dopa response for five years or more.
- Clinical course of ten years or more.
- Hyposmia. = reduced ability to smell
- Visual hallucinations.
Give some differentials for PD
benign essential tremor drugs or toxins post encephalitis huntingdon's disease wilson's disease corticobasal generation mulit-onfarct dementia lewy-body dementia pick's disease cerebellar tremor psychogenic tremor multiple system atripy progressive supranuclear palsy
What is the difference between PD and benign essential tremor
in BET, tremor is worse on movement (eg, while trying to hold a cup of tea) and rare while at rest.
Which drugs or toxins can cause PD like symptoms
SSRIs caffeine, amfetamines, beta-adrenergic blockers, tricyclics, lithium. Neuroleptics (eg, haloperidol, chlorpromazine) anti-emetics (eg, prochlorperazine)
What is the difference between PD and Huntingdon’s disease
present earlier with rigidity instead of chorea
Normally, there is family history
What is the difference between PD and Wilson’s disease
in W - earlier onset with characteristic Kayser-Fleischer rings and hepatitis.
What is the difference between PD and corticobasal degeneration
manifest by obvious signs of cortical dysfunction - eg, apraxia, dementia and aphasia.
What is the difference between PD and multi-infarct dementia
characterised by:
cognitive impairment,
spasticity, and
extrapyramidal signs.
What is the difference between PD and Pick’s disease
affects the frontal and/or temporal lobes.
Level of consciousness is not affected (unlike in Alzheimer’s disease)
Parkinsonism is usually mild
What is the difference between PD and a cerebellar tremor
unilateral or bilateral, low-frequency intention tremor.
It may be caused by stroke, brainstem tumour, or multiple sclerosis.
What is the difference between PD and psychogenic tremor
variable,
increases under direct observation,
decreases with distraction
changes with voluntary movement of the contralateral limb.
What is the difference between PD and multiple system atropy
Parkinsonian symptoms, often with a poor or temporary response to levodopa therapy.
more severe/early onset autonomic dysfunction (postural hypotension/erectile dysfunction).
What is the difference between PD and progressive supranuclear palsy
characterised by paresis of conjugate gaze with initially problems looking up and down on request, (vertical plane)
advancing to difficulty in following objects up and down.
Describe the physiology behind the treatment of parkinson’s disease
The symptoms of Parkinson’s appear when dopamine levels become too low.
Most drug treatments work by:
• increasing the amount of dopamine in the brain
• acting as a substitute for dopamine by stimulating the parts of the brain where dopamine works
• blocking the action of other factors (enzymes) that break down dopamine
When is levodopa + carbidopa treatment offered to patients
when motor symptoms decrease their quality of life
What are the different actions of levodopa and carbidopa
Levodopa crosses BBB and is converted to dopamine
carbidopa is an inhibitor of DOPA decarboxylase that is unable to cross BBB. Therefore prevents peripheral SE.
What drugs can be given to patients with PD whose motor symptoms do not affect their quality of life
levodopa,
non-ergot-derived dopamine-receptor agonists (pramipexole, ropinirole or rotigotine)
monoamine-oxidase-B inhibitors (MAO-B normally degrades dopamine) (rasagiline or selegiline hydrochloride).
Describe how deep brain stimulation works in PD
- Electrodes are placed in the basal ganglia and attached to an internal stimulator, which is placed subcutaneously below the clavicle.
- May be used to provide unilateral or bilateral stimulation.
- It may reverse akinesia, rigidity and tremor.
When should deep brain stimulation for PD be considered?
people with advanced Parkinson’s disease whose symptoms are not adequately controlled by best medical therapy
What are some complications of deep brain stimulation
intracerebral haemorrhage and confusion
What are some complications of dopamine therapy for PD
motor complications - dyskinesia, involuntary movements
response fluctuation
end of dose deterioration
more common with dopamine receptor agonists:
sleepiness
hallucination
impulse control disorders
What is it especially important to ask about before prescribing any dopamine therapy in PD
history of previous impulsive behaviours, alcohol consumption, or smoking.
due to risk of impulse control disorders
How are impulse control disorders due to PD therapy managed
dopamine-receptor agonist therapy may be reduced or stopped
doses should be reduced gradually and patients should be monitored for symptoms of dopamine agonist withdrawal.
Specialist cognitive behavioural therapy should be offered if modifying dopaminergic therapy is not effective.
Which features of PD do not respond to dopamine therapy
Axial problems - balance, speech and gait disturbance
What common complications occur due to PD
- Infections.
- Aspiration pneumonia.
- Bed sores.
- Poor nutrition.
- Falls.
- Contractures.
- Bowel and bladder disorders
Which members of the MDT can be especially helpful in PD
SALT
OT
PT
What is the difference between PD and drug induced parkinsonism?
motor symptoms are generally rapid onset
bilateral rigidity and rest tremor are uncommon
What are the key side effects of levodopa
reduced effectiveness with time (usually by 2 years)
unwanted effects: dyskinesia (involuntary writhing movements), ‘on-off’ effect, dry mouth, anorexia, palpitations, postural hypotension, psychosis, drowsiness
no use in neuroleptic induced parkinsonism
What are the key side effects of dopamine receptor agonists
pulmonary, retroperitoneal and cardiac fibrosis - echocardiogram, ESR, creatinine and chest x-ray should be obtained prior to treatment and patients should be closely monitored
impulse control disorders
excessive daytime somnolence
hallucinations in older patients
What problem can acute withdrawal of levodopa cause?
precipitate neuroleptic malignant syndrome.
How is the AMT calculated
- What is your age?
- What is the time to the nearest hour?
- Give the patient an address, and ask him or her to repeat it at the end of the test
e. g. 42 West Street - What is the year?
- What is the name of the hospital or number of the residence where the patient is situated?
- Can the patient recognise two persons (the doctor, nurse, home help, etc.)?
- What is your date of birth? (day and month sufficient)
- In what year did World War 1 begin? (1994)
- Name the present monarch/prime minister/president.
- Count backwards from 20 down to 1.
what are the features of a cerebellar lesion
Dysdiadokinesis/dysmetria Ataxia Nystagmus Intention tremor Slurred staccato Hypotonia
When someone has a TIA, how soon should they be seen in a TIA clinic
Depends on ABCD2 score: Age >60 = 1 BP >140/90 = 1 Clinical features No weakness, speech = 1 UL weakness = 2 Duration of symptoms 10min – 1hr = 1 >1hr = 2 DM = 1
<4 = TIA clinic <1wk ≥4/crescendo = TIA clinic <24hrs
What management is put into place before someone is seen in a TIA clinic
Aspirin 300mg (then 75mg/d)
Statin
ECG
Which drugs are CYP450 inducers
PC BRASS” ↓ levels of crime
Phenytoin Carbamazepine Barbiturates Rifampicin Alcoholic (chronic) Smoking St. John’s Wort
Which drugs are CYP450 inhibitors
“AAASS IF” it will, it will actually ↑ levels ABx (macrolide, quinolone) Antacids (omeprazole) Alcohol binge Sodium valproate SSRI Isoniazid Fluconazole
