medical school mindmap

1. Parkinson's disease
Learning objectives:
Know the
differences between
Parkinson ’s disease
and parkinsonism
Describe the
features of Parkinson
’ s disease
Principles
management of
Parkinson ’ s
disease
epidemiology
majority idiopathic
symptoms begin
55-60 yrs
1% of over 60 year olds
M:F=1.5:1
2nd most common
neurological disorder
greatest prevalence in US
pathophysiology
loss of pigmentted
dopaminergic
neurones in
substantia niagra
presence of lewy
bodies withing
pigmented neuron
60-80% neurones
are lost before the
motor signs emerge
braak staging 1-6
correlates with
clinical manifestation
of disease
scientifically
basal ganglia
=caudate nucleus+globus pallidus
controlling voluntary
movements and
establishing postures
if altered->unwanted
movements
substantia niagra
important motor centre
projects to caudate and
putamen(2 nuclei of the
basal ganglia that
together comprise what is
called the striatum)
these NIGROSTRIATAL
cells use neurotransmitter
DOPAMINE and cells
within niagra produce
dopamine normally
lesion site in
PD-degeneration of the
melanin-containing cells
absence of the transmitter
produces the crippling
features of PD
motor circuit
modulates output from
the motor cortex
loss of substantia niagra
results in dysfunctional
stimuli to basal ganglia
imbalance of excitatory
and inhibitory pathways
regulating movement-->
symptoms seen in PD
Subtopic
causes
clinical findings
cardinal motor
symptoms
tremor
pill rolling
unilateral
rapid at rest
increased with stress
frequency of 4-5 Hertz
bradykinesia
slowness of movement
difficulty initiating
voluntary movement
difficulty with sequential
complex movements
decreased amplitude of
movement(writing)
rapid fatigability of
repetitive movements
rigidity
increased resistance of
relaxed muscle to passive
stretch
commonly asymmetrical
cogwheel(tremor and rigidity
lead pipe
postural instability
balance well preserved
until later stages
shuffling gait and poor
arm swing contribute
high falls risk
clinical assessment
on reviewing patients
always assess for motor
and non motor symptoms
and signs
motor symptoms
function
poor bed mobility
diffuculty with transfers
poor
dexterity/coordination
micrographia
painful dystonia
face
hypophonia
dysphagai/drooling
hypomimia
gait
shuffling gait
flexed axial posture
festination
decreased arm swing
turning 'en bloc'
freezing
falls
non motor symptoms
depression
cognitive decline
dementia~30%
executive dysfunction
sleep disturbance
insomnia
daytime
somnolence/fatique
vivid dreams
hallucinations
sensation
orthostatic hypotension
impaired proprioception
autonomic
seborrhoeic dermatitis
urinary incontinence
constipation
sweating abnormalities
diagnosis
med. Hx and clinical
examination(triad)
observation
no lab tests
CT and MRI brain
usually unremarkable
MRI can outrule
multi-infarcts,
hypdrocephalus and
wilsons
PET/SPECT useful in
atypical cases
diff. Dx
essential tremor
vascular parkinsonism
drug-induced
parkinsonism
parkinsonism in parkinson
plus syndrome
multi systems atrophy
postural instability with falls
postural hypotension
bladder dysfuntion
pyramidal signs
cerebellar signs
progressive supranuclear palsy
parkinsonism(symmetrical)
paralysis of upward gaze
dementia
personality changes
speech difficulties
thyrotoxicosis
management
aims
educate and support
preserve function
maintain general health
and fitness
treat other medical
problems
non-pharmacological
PD supprt group
physiotherapy and
occupational therapy
SALT and dietician and MSW
communication with GP
pharmacological
aims to control
signs/symptoms for as
long as possible while
minimising adverse effects
replacement of dopamine
def is the key to therapy
aim to stable stimulation
of brain dopamine
receptors
prevent breakdown of
dopamine in CNS
monoamine oxidase
inhibitor(MOAB)
selgiline
rasagiline
S/E
orthostatic hypotension
insomnia
Catechol-O-methyl
transferase(COMT)entacopone
Levodopa and
DCI(benserazide or
carbidopa)
mainstay of treament in PD
most effective for initial
therapy >70 yrs
greatest benefit with
fewest S/E short term
restore normal function
using minimum dose of
levodopa
pre meals on empty
stomach gives better
absorption
domperidone for transient
nausea when start
treatment
long term troublesome S/E
motor fluctuation(on-off
phenomenon)
dyskinesia(chorea or
dystonia)
peak dose dyskinesia
add dopamine agonist,
COMT inhibitor, MAO-B
slowly lower the dose of levodopa
refractory
symptoms-apomorphine(dopamine
agonist is useful
britajet(subacute as needed)
subcut
infusion(hospitalised prior
to this)
anticholinergic for
tremor/drooling
procyclidine
biperidin
S/E
confusion, memory
impairment, blurred vision
etc
dopamine agonist
ropinerole
pramipexole
apomorphine
helps delay use of
levodopa in young pts and
useful as add-on therapy
in late disease
S/E
OH, hallucination, nausea,
oedema, sleep attacks
surgery
thalamotomythalamusreduces tremor
pallidotomy
globus pallidus
reduces tremor, rigidity,
bradykinesia and
dyskinesia
deep brain stimulation
surgical treatment
involving the implantation
of a medical device called
a brain pacemaker, which
sends electrical impulses
to specific parts of the
brain
need
a clear diagnosis of PD
levodopa responsive pts
with motor fluctuations or
dyskinesia
no psychiatric probs
good insight into risk
benefit of this treatment
- - Mindjet