Neurology Flashcards
(148 cards)
1
Q
Name the upper limb and lower limb dermatomes
A
Upper - C5-T1
Lower - L1-S1
2
Q
What would be the difference in examination findings of someone with Bell’s palsy and someone who has had a stroke?
A
Bell’s palsy (LMN lesion) - complete facial paralysis on one side
Stroke (UMN lesion) - forehead movements are spared due to bilateral innervation of the upper branches of CNVII
3
Q
In a CNX palsy, which side would you expect the uvula to deviate?
A
Deviate away from the side with the lesion
This is because the “pulling” muscles of the same side (ipsilateral) are disabled
4
Q
In a CNXII palsy, which side would you expect the tongue to deviate to?
A
Deviate towards the side with the lesion
This is because the “pushing” muscles of the same side (ipsilateral) are disabled
5
Q
What does the pronator drift sign indicate?
A
Upper motor neuron lesison
Lesion in the pyramidal tracts
6
Q
How can you tell the difference between rigidity and spasticity in a patient with increased tone on examination?
What do each suggest?
A
Rigidity - tone remains stiff through tough entire movement, regardless of speed. Suggests extra pyramidal lesion (e.g lead pipe rigidity seen in Parkinson’s)
Spasticity - stiffness is velocity dependant, and is exacerbated by attempt to move limb quickly. Suggests pyramidal lesion
7
Q
How can you illustrate clonus, what does this suggest?
A
Briefly dorsiflex the foot
If the foot plantarflex’s in a “beating” motion this is clonus
If you can illustrate this more than 3x, it suggests an UMN lesion
8
Q
How is power graded on neurological examination?
A
0 - no power
1 - twitching, no movement
2 - movement, but cannot overcome gravity
3 - movement can overcome gravity
4 - movement against resistance but weaker
5 - normal muscle strength
9
Q
What does it mean if the plantar’s are “up going” or “down going”
A
Observation of toes when object is run along plantar aspect of foot
Up going - upper motor neuron pathology
Down going - normal
10
Q
What does impaired vibration sensation suggest?
A
Pathology in dorsal columns of spinal cord
11
Q
What does impairment pinkprick sensation suggest?
A
Pathology in the spinothalamic tracts of the spinal cord
12
Q
How does the differential diagnosis vary in neurology dependant on the onset of symptoms?
A
Sudden events - vascular (infarction, ICH, SAH)
Acute onset (mins-hours) - infections (meningitis, encephalitis)
Subacute (days-weeks) - autoimmune (MS)
Chronic (months, years) - genetic, neurodengerative (Parkinson’s), neoplastic
13
Q
What are the UMN signs found in neurology?
A
Weakness (pyramidal signs) Increased tone (Spasticity and rigidity) Up going plantars Hyperreflexia Pronator drift
14
Q
What are the LMN signs found in neurology?
A
Muscle wasting Fasciculations (receptor induced contractions) Focal weakness Hyporeflexia Reduced tone
15
Q
What is the difference between the pyramidal tracts and the extrapyramidal tracts?
A
Both are motor descending pathways
Pyramidal control voluntary movements (e.g, corticospinal)
Extrapyramidal control involuntary and fine tuning movements (E.g, basal ganglia, cerebellum))
16
Q
What is pyramidal pattern weakness?
A
Upper limbs: extensors weakened more than flexors
Lower limbs: flexors weakness more than extensors
17
Q
What are extrapyramidal signs?
A
Involuntary movements
Tremors
Muscle contractions
18
Q
What are the main sensory ascending tracts and what information do they carry?
A
Spinothalamic tracts - touch, pressure, pain, temp
Dorsal columns - vibration, proprioception
19
Q
Where do the spinothalamic and dorsal columns tracts dessucate?
A
Spinothalamic - dessucates immediately and travels up contralateral side to thalamus
Dorsal columns - travels up ipsilateral side, and desscuates at the medulla, before traveling to thalamus on contralateral side
20
Q
What is the main motor descending pathway
A
Corticospinal tract
21
Q
What is brown sequard syndrome?
A
Where you get different neurological symptoms because of a hemi section of the spinal cored . This is due to how the tracts dessucate? Below level of damage you would see:
- Ipsilateral UMN signs (corticospinal tract damage)
- Ipsilateral loss of vibration and proprioception (dorsal columns damage)
- Contralateral loss of pain and temp (spinothalamic damage)
22
Q
What is the difference between a bulbar and psudobulbar palsy?
A
Bulbar palsy - LMN palsy affects IX, X, XI and XII cranial nerves
Will have LMN signs like tongue wasting
Psuedobulbar palsy - UMN that affects the corticobulbar tracts of the V, VII, IX, X, XI and XII cranial nerves
Will have UMN signs like exaggerated jaw jerk
23
Q
What are the 4 types of motor neuron disease?
A
Amyotrophic lateral sclerosis (ALS) - (most common) limbs initially affected
Progressive bulbar palsy (PBP) - speech and swallowing affected initially
Progressive muscular atrophy (PMA) - LMN affected only
Primary lateral sclerosis (PLS) - UMN affected only (rare disease)
24
Q
How does motor neuron disease present?
A
Usually begins by affecting a single limb or aspect of motor function, then becomes more generalised as the disease progresses
People initially only have LMN or UMN signs but typically develop a combination of both as the disease progresses
25
What are the 3 P’s of motor neuron disease?
Painless
Progressive
Pure motor symptoms
26
What is motor neurone disease (MND)?
A disease in which the motor neurons are degenerated
Motor neurons control the muscles which control movement, speech, breathing and swallowing
As these neurons die muscles gradually weaken and waster, this can cause a pattern of weakness
Can affect both UMN and LMN or just one set
27
What medication is licensed for use in amyotrophic lateral sclerosis (ALS) and progressive bulbar palsy (PBP)
How does it work?
Riluzole
Prevents stimulation of glutamate receptors, which helps slow down the motor neuron death
28
How would you exaggerate the tremor seen in Parkinson’s disease?
Tremor is moist easily seen when patient is distracted
| Get the patient to count back from 20 seconds
29
How would you examine a Parkinson’s patient for bradykinesia?
Get the patient to continually snap their fingers and see if the movement slows down
30
What are the main symptoms of motor neuron disease?
Muscle weakness and fasciculations
Mixture of upper and lower motor neuron signs
Wasting of small hand muscles/tibilais anterior is common
LACK OF SENSORY SIGNS/SYMPTOMS
31
Which type of dementia is motor neuron disease associated with?
Frontotempral dementia
32
What is the prognosis for motor neuron disease?
50% of patients die within 3 years
33
How are the respiratory symptoms of motor neuron disease managed?
Non invasive ventilation (BIPAP) used at night
34
Which type of motor neuron disease carries a genetic link?
Amyotrophic lateral sclerosis
In familial cases the gene lies on chromosome 21 and codes for superoxide dismutase
35
Which type of motor neruon disease carries the worse prognosis?
Progressive bulbar palsy
36
Which type of motor neuron disease carries the best prognosis?
Progressive muscular atrophy
37
What is the differential diagnosis for a patient presenting with weakness in all 4 limbs?
UMN cause - acute cervical myelopathy e.g, transverse myelitis
LMN cause - guilian barre syndrome
Mixed UMN and LMN - motor neuron disease
38
What is guillian barre syndrome?
Demyelinating disease of the peripheral nervous system
Characterised by symmetrical cranial or limb weakness
39
What causes guillian barre syndrome?
Usually triggered by infection (most common campylobacter)
This triggers molecular mimicry to occur and for the body to start attack the myelin sheath of peripheral nerves
40
How does GBS usually present?
Initially sensory symptoms (paraesthesia and pins and needles)
Motor symptoms - muscle weakness usually beings in the legs (weakness is classically ascending)
Can get cranial nerve involvement - difficulty speaking, facial muscle weakness
Can get respiratory involvement if respiratory muscles are affected
41
What is the most common type of GBS?
Acute inflammatory demyelinating polyradicuoneuropathy (AIDP)
42
What is miller-fisher syndrome?
```
Type of GBS
Consists of a triad of:
- ophthalmoplegia
- areflexia (loss of reflexes)
- ataxia (loss of balance)
```
43
How is GBS diagnosed?
Lumbar puncture - CSF will show cytoalbuminologic dissociation
(Normal WBCs, elevated protein)
Nerve conduction studies - can point to diagnosis
44
What are the typical lumbar puncture findings in someone with GBS?
```
Cytoalbuminologic dissociation
Normal WCC (<5)
Raised protein (>0.45)
```
45
How would you monitor someone’s respiratory function with GBS?
Pulmonary function tests
| FVC should be monitored regularly
46
How is GBS managed?
Intravenous immunoglobulins - reduce the immune response
Plasmapheresis - plasma is filtered from the blood to help remove the autoantibodys
47
What is the prognosis of GBS?
Individuals make a slow recovery over several months as there is regrow the of the myelin on the peripheral nerves
48
How does subacute combined degeneration of the spinal cord present?
Dorsal columns affected - loss of proprioception, light touch and vibration
Lateral corticospinal tract affected - causes spastic weakness and up going plantars (UNM signs)
Damage to peripheral nerves - results in LMN signs
49
What causes subacute combined degeneration of the spinal cord?
Vitamin B12 deficiency
50
What is Bell’s palsy?
Temporary weakness affecting one side of the face
| Due to a lesion in the facial nerve
51
How does Bell’s palsy differ from a stroke?
Bell’s palsy is complete weakness of one side of the face whereas stroke spares the muscles above the eyebrow
Bell’s palsy is more gradual onset (hours-days) - stroke is more sudden
Bell’s palsy symptoms are purely limited to facial movement
Bell’s palsy may come with some prodromal symptoms
52
What are the prodromal symptoms that can occur with Bell’s palsy?
Pain behind the ears
Hearing or taste changes
Strange feeling in the face
53
What is the cause of Bell’s palsy?
Cause is unknown
| Viral aetiology suspected, but unproven
54
How is Bell’s palsy managed?
Prednisolone - 7 day 60mg course given within 3 days of symptoms
Acyclovir - some doctors use, but evidence is week
Eye drops - to stop affected eye drying out
55
What is the progression and prognosis of Bell’s palsy?
Symptoms worsen over first few days
Recovery can take 4-6 months
Majority of cases make full recovery
The time taken to recovery relates to severity of initial weakness
56
What is Ramsay Hunt Syndrome?
Shingles infection that affects the facial nerve
| Caused by herpes zoster infection of the geniculate ganglion of the facial nerve
57
How does Ramsay hunt syndrome present?
Painful vesicles around affected external ear, can also get them in inside the mouth
Weakness of affected side of face causing facial drooping
Altered taste on affected side of tongue
58
How is Ramsay hunt syndrome investigated?
MRI - to look for inflammation along facial nerve
| Nerve conduction studies - to assess damage to facial nerve
59
How is Ramsay hunt syndrome managed?
Antivirals (Acyclovir)
| High dose steroids
60
What is the prognosis of Ramsay hunt syndrome?
If antiviral treatment given within 72 hours of developing symptoms, then approximately 70% will make a full recovery
61
What is footdrop?
Drooping of the forefoot due to weakness, irritation or damage to the nerves
Causes weakness of the foot and causes it to “slap” the ground
62
What are two main differentials for footdrop?
Common peroneal nerve palsy
| Lumbar root lesion (radiculopathy) - due to slipped disc at L4/L5
63
What is the pathophysiology of a common peroneal nerve palsy?
The common peroneal nerve winds around the fibular head
| It is susceptible to compression at this site, especially in the setting of prolonged/repeated knee flexion
64
How does a CPN palsy cause foot drop?
The common peroneal nerve innervates the tibilalis anterior which is responsible for dorsiflexion
65
How does a prolapsed intervertebral disc at L4/L5 cause foot drop?
Slipped discs compress posterior laterally
Results in compression of the L5 root
L5 root contributes to multiple nerve fibres in the leg, one being the fibres to tibilais anterior (which causes foot dorsiflexion)
66
How can you differentiate between the two main causes of foot drop? (CPN palsy and slipped disc)
In CPN palsy, the foot will still be able to invert, and the ankle reflex will be spared. CPN palsy is usually painless
In a lumbar radiculopathy, there will be weakness of both inversion and eversion of the foot. There may also be loss of ankle reflex as an L5 root compression severe enough to cause a foot drop will almost always involve the S1 root (which is responsible for the ankle reflex)
Also in a slipped disc you would get back pain
67
What are the important questions to ask someone presenting with foot drop?
Ask about back pain
Ask about paresthesia, numbness and tingling
Any bowel or bladder involvement
Any history of trauma to the lumbar spine?
Any unusual activity prior to onset of symptoms
68
How is footdrop managed?
Footdrop splint
69
What is the prognosis of CPN palsy and how is this determined
Depends on degree of nerve damage - this can be found out by doing nerve conduction studies to look at the degree of damage to the myelin sheath
Can also do EMG to look for any axonal damage (this is associated with poorer prognosis)
70
What is the clinical presentation of a radial nerve palsy?
Wrist drop
71
How is CPN palsy diagnosed?
Nerve conduction studies
72
How is CPN palsy managed?
Foot splint to help with foot drop
| Obstain from activities which could compress the common peroneal nerve e.g, kneeling
73
What is neuromyelitis optica (NMO)?
A rare autoimmune condition that affected the spinal cord and the nerves of the eyes
It causes transverse myelitis (inflammation of the spinal cord) and also causes optic neuritis (inflammation of the optic nerve)
74
What is the main differential diagnosis for multiple sclerosis?
Neuromyelitis Optica
75
What is multiple sclerosis?
Autoimmune disease of CNS
| Caused by inflammation, demyelination of the nerves in the brain and spinal cord
76
Which gender is MS more common in?
Women 3:1 ratio
77
What are the risk factors for developing MS?
Low vitamin D
Virus exposure early in life e.g, measles, rubella, mumps - can trigger autoimmune response
Smoking
Obesity
Genetic factors - certain genes may predispose
78
What are the different types of MS?
Relapsing remitting - symptoms worsen during relapses
Primary progressive - gradual progression of disease
Secondary progressive - relapsing remitting followed by steady progression
Progressive relapsing - progressive disease, with sudden relapses
79
What is the most common type of MS?
Relapsing remitting
80
How often do patients with MS typically relapse?
On average, patients have one relapse every 2 years
81
What is the pathophysiology of relapsing remitting MS?
During relapse, the immune system is active and attacks the oligodendrocytes producing the myelin sheath, destroying it and causing symptoms to worse as the nerve signals are broken
During remitting, the immune system is dampened down and new myelin is able to form around the axons
Overtime, as oligodendrocytes become more damaged, the remyelination will stop and damage will become irreversible
82
How does MS typically present?
Optic neuritis symptoms - usually these are the first symptoms
Fatigue
Numbness and tingling
UMN weakness signs
Gait difficulties - due to weakness, loss of balance and fatigue
Bladder and bowel problems
83
What are the signs and symptoms of optic neuritis?
Pain on eye movement
Blurring of vision
Swelling of optic disc
Uhthoff’s phenomenon - worsening of vision during fever, hot weather or exercise
Relative Afferent pupillary defect (RAPD)
84
How is MS investigated?
Bloods - baseline, B12, viral serology (HIV, syphillis, hep b, hep c), NMO/aquaporin antibodies, bloods to look for autoimmune diseases (ANA, ENA, dsDNA, ANCA)
MRI - to look for areas of demyelination
CSF - will show oligoclonal IgG bands on electrophoresis
VEP (visual evoked potential) - to look for impaired transmission along the optic nerve
85
How is MS diagnosed?
Need two separate attacks at two different places (in the CNS) and two different times (months apart)
86
What is a clinically isolated syndrome?
This is when a patient only has one episode of MS symptoms
87
How is MS managed?
High dose corticosteroids - IV 1g OD methyprednisolone given for 3 days during relapses
Disease modifying agents (DMTs) - given between relapses to help reduce the number of relapses. These help dampen immune system
Drugs to control symptoms - e.g, baclofen, gabapentin, sertraline, oxybutinin
88
What are the common disease modifying agents used in MS?
Interferon beta
Natalizumab
Alemtuzumab
89
When someone presents with gait ataxia (unsteadiness of gait),what are the different areas in the nervous system could this be originating from?
Cerebellum (cerebellar ataxia) - would show cerebellar signs e.g, dyskensia, pass pointing
Dorsal columns of spinal cord (sensory ataxia) - would also show signs of sensory disturbance e.g, romberg’s test positive, pins and needles
Peripheral nerves roots (sensory ataxia) - would show signs of spinal cord compression e.g bladder symptoms
Vestibular apparatus (vertigo) - patients describe spinning worse with head movement, nausea can be present
90
What is L’Hermitte’s phenomenon?
Symptom of MS
Sudden electric shock like sensation radiating down and up the spinal column provided by flexion or extension of the neck
Can also get shock symptoms in arms and legs
Can get a band link sensation around the upper chest
91
What tests need to be done before giving high dose steroids in MS and why?
Check for signs of systemic infection
- take general history
- do routine bloods (FBC, u+E, glucose)
- do urine dip
92
What is rapidly evolving severe MS?
Very active form of MS
| These patients are candidates for a newer monoclonal antibody treatment
93
Which MS patients should be taking disease modifying agents?
Patients who are experiencing two or more significant relapses over a 2 year period
They are not suitable for patients with progressive MS
94
What are the main causes of funny do’s?
Syncope
Seizures
Psychogenic non epileptic attacks
95
What is syncope?
Loss of consciousness caused by lack of cerebral blood supply
96
What are the different types of syncope?
Vasovagal - drop in BP when altering position
Cardiogenic - abnormal heart rate/rhythm causing drop in BP
Micturition - when passing urine
Simple orthostatic hypotension - syncope when standing
97
How would you differentiate vasovagal syncope from other types of funny do’s?
3 P’s:
position - only occurs when upright
provoking factor - pain, emotional shock, dehydration
prodrome - symptoms before e.g, dizziness, visual blurring
Recovery from vasovagal is quick (within mins), patients may become pain and experience some jerking of limbs
Note that urine incontinence can be present (especially in women)
Tongue biting is uncommon in vasovagal syncope
98
How would you differentiate epilepsy seizures from other types of funny do’s?
Tongue biting, incontinence
Brain fog - patients will struggle to remember events prior to fit
Prolonged limb jerking
Longer period of confusion following event (15-30 mins of drowsiness)
Patients can have deja vu prodromal symptoms
99
Which type of epilepsy is more common in patients who had febrile convulsions at a young age?
Mesalazine temporal sclerosis
100
What is a Jacksonian march in epileptic fits?
Where jerking movements start in one muscle group and then spread to others
101
What is Todd’s palsy?
Weakness in arms/legs after a focal seziure in the motor cortex which can last up to 2 days
102
What is the difference between a partial seizure and a primary generalised seizure?
Partial seizure - focal onset, referable to one side of hemisphere in a single lobe
Primary generalised seizures - simultaneous onset of electrical discharge throughout cortex, both hemispheres are affected
103
What is the difference between a simple partial seizure and a complex partial seizure?
Simple - patient conscious with focal motor or sensory symptoms
Complex - patient unconscious and unaware with focal motor or sensory symptoms
104
Which lobe do complex partial seizures usually occur in and what are the symptoms?
Temporal lobe
- automatism (lip smacking, playing with tie, picking at clothes, scratching at leg, repetition of a phrase, getting undressed)
- inappropriate laughing
- auditory hallucinations
105
What is the most common type of primary generalised seizures?
Tonic-clonic
LOC, limbs stiffen (tonic) then jerk (clonic)
106
How would you investigate a seizure?
Baseline bloods
ECG - look for cardiogenic causes e.g, prolonged QT
MRI - to look for tumour causing, usually only done if evidence from neurological exam is present
EEG - look for electrical signals in the brain
107
What are the main drugs used in the management of epilepsy?
Lamotrigine
Carbamazepine
Sodium valproate (should be avoided for women of childbearing age)
108
Which antiepileptic medication is best to use in pregnancy?
Lamotrigine
109
What is the risk of taking antiepileptic drugs during pregnancy and how is this managed?
Risk of neural tube defects
Mothers should take 5mg of folic acid prior to conception and throughout 1st trimester
110
What are the rules surrounding epilepsy and driving?
Must inform the DVLA if you have a seizure
If seizure is one off - can reapply for license in 6 months
If multiple seizures - then can reapply if seizure free for one year
If switching drugs - recommenced to stop driving during changeover period and 6 months after
Can be fined if you don’t tell the DVLA about seizures, and prosecuted if involved in an accident. Doctors can break confidentiality if they know they are still driving and cannot be purse used to inform the DVLA. Must inform patient you are going to do this.
111
How many drugs should you take to manage epilepsy at a time?
One drug
Try one at a time and if it doesn’t work then come off slowly while titrating in the 2nd drug to avoid breakthrough seizures
112
What is medically refractory epilepsy?
Where seizures are unable to be managed with at least two different anticonvulsants
113
What is status epilepticus?
Seizure ongoing for >5 mins
Medical emergency
Can cause neuronal death and patients are unable to recover
114
How is status epilepticus managed?
1st line - benzodiazepines
- IV lorazapam (hospital) IM midazolam, rectal diazepam (community)
2nd line - IV antiepileptic e.g, IV phenytoin (hospital setting)
3rd line - anaesthesia, intubation and ventilation
115
What is SUDEP?
Sudden unexplained death in epilepsy
1 in 1000 people with epilepsy die from SUDEP each year
Risk is increased in patients who have uncontrolled seizure disorder
116
What acute underlying causes do you need to rule out in someone presenting with a seizure?
Stroke, haemorrhage
Infection - meningitis, encephalitis
Metabolic disturbance - hypoxia, sodium/calcium/glucose imbalance
117
How do you differentiate non epileptic attack disorders from other causes of funny do’s?
Prolonged seizures/shaking lasting more than 5 mins (remember to rule out status epilepticus)
Prolonged unresponsiveness ‘pseudo sleep’
118
Which patients with epilepsy would benefit from brain surgery?
Those with a known underlying brain abnormality which is causing the increase in seizure threshold
119
What is the difference on examination between a Parkinsonism tremor and a drug induced Parkinsonism tremor?
Parkinsonism - tremor worse at rest, unilateral symptoms
| Drug induced tremor - tremor usually rapid onset and bilateral, rest tremor is uncommon
120
Which types of tremor are worse on movement?
Essential tremor
Drug induced tremor
Hyperthyroidism
121
How do you differentiate an essential tremor from other types of tremor?
Essential tremor is usually familial
Tremor is typically worse on movement (when trying to eat or drink)
Tremor usually present in legs or jaw
No evidence of bradykinesia or gait disorder
122
What is the clinical triad or Parkinsonism?
Resting tremor
Bradykinesia
Rigidity
123
What is the difference between Parkinson’s disease and parkinsonism?
Parkinsonism - a general term that refers to a group of neurological disorders that cause movement problems similar to those seen in Parkinson’s disease such as tremor, bradykinesia and rigidity
Parkinson’s disease - a neurodegenerative brain disorder causing Parkinsonism symptoms as well as a range of non motor symptoms e.g, depression, cognitive changes
124
What are the different causes of Parkinsonism?
```
Parkinson’s disease
Vascular Parkinsonism
Dementia with Lewy bodies
Drug induced Parkinsonism
Multi system atrophy
Progressive supranuclear palsy
Corticobasal degeneration
```
125
How would you differentiate drug induced parkinsonism from other causes of Parkinsonism?
History of antipsychotic use (dopamine blockers)
| History of stimulants use e.g amphetamines, cocaine
126
What is progressive supranuclear palsy (PSP)?
Rare progressive condition causing problems with balance, movement, vision, speech and swallowing
Due to accumulation of tau protein in brain
Occurs in people aged over 60 years
Presents with Parkinsonism symptoms
Patients have a vertical supranuclear gaze palsy
127
What will an MRI scan show on a patient with progressive supranuclear palsy?
Reduction of brain volume (humming bird sign)
128
How do you differentiate multiple system atrophy (MSA) from other causes of parkinsonism?
MSA affects the autonomic nervous system - so patients will also have bladder problems e.g urgency, hesitancy or incontinence
Patients may also have orthostatic hypotension - where BP drops on standing
129
How can you differentiate vascular Parkinsonism from other causes of parkinsonism?
Usually caused by multiple mini small strokes in the brain
Patients tend to have more problems with gait and tremor and have more lower body symptoms
Disorder progresses very slowly compared to other types of parkinsonism
130
What is the pathophysiology of idiopathic Parkinson’s disease?
Misfolded alpha synuclein proteins accumulate to make Lewy bodies in the substantia nigra
This leads to degeneration of dopaminergic neurons in the substantia nigra pars compacta
This results in the underproduction of L-DOPA, which is needed for coordinated movement
131
What are the risk factors for Parkinson’s disease?
Increasing age
Environmental exposure to pesticides, rural living and drinking well water
Thought that exposure to toxins/infective agents can spread to the brain
132
How does idiopathic Parkinson’s disease usually present?
Tremor, rigidity, bradykinesia, gait impairment
Usually presents more prominent on one side
133
How does someone’s writing with Parkinson’s change?
Micrographia
Where writing becomes small and spidery - tending to tail off
134
What are the characteristics of a Parkinson’s disease tremor?
Resting tremor - that improves with movement
Tremor can be made more apparent by getting patient to concentrate on someone else (e.g, count down from 20-1)
Pill rolling tremor in hand - looks like they are rolling a pill between thumb and finger
135
What is plastic rigidity and how can this be exaggerated on examination?
Where there is an increase in tone when the joint it moved slowly and gently
This can be increased by getting the patient to move the opposite limb e.g, tone in arm increased when other other is moving up and down
136
How can bradykinesia be demonstrated on examination?
Asking patients to put thumb and fingers together repetitively
Asking patients to tap foot on floor repetitively
After some time you should see the movements slow in pace
137
What are the gait changes seen in Parkinson’s disease?
Stooping
Hurrying gait - takes time to start then speeds up
Shuffling gait
Poor arm swinging
Impaired turning - patients struggle to turn
Freezing - this is exacerbated by doorways, patterned carpets and other obstructions
138
What genes have been assocaited with Parkinson’s disease?
Parkin
SNCA
LRRK2
139
How are the direct and indirect pathways in the basal ganglia affected in Parkinson’s disease?
```
Direct pathway (responsible for initiating movement) - in Parkinson’s disease there are reduced excitatory signals in the direct pathway causing it to become overactive
Indirect pathway (responsible for dampening movement) - in Parkinson’s there are reduced inhibitory signals in the indirect pathway causing it to become overactive
The net effect of this is there is too much inhibitor output from the basal ganglia leading to reduced movement
```
140
What are the non motor symptoms of Parkinson’s disease which can commonly present 5-10 years before the onset of motor symptoms?
R.E.M sleep disorders
Anosmia (loss of smell)
Constipation
Depression
141
In someone presenting with Parkinson like symptoms, what are the signs which may point you away from Parkinson’s disease?
If there is symmetrical onset - as Parkinson’s disease is usually asymmetrical
Early gait abnormalities - this is usually a late sign in Parkinson’s
Pyramidal tract signs (UMN signs) - as Parkinson’s is extrapyramidal
Hx of strokes or antipsychotic mediation
If there is a poor levodopa response
142
What investigations are done to help support diagnosis in Parkinson’s and Parkinsonism?l
SPECT
| PET scan
143
What is the usual 1st line drug regime given in a patient with Parkinson’s disease?
Levodopa (L-DOPA)
Carbidopa
Commonly seen as co-beneldopa together
144
Why is levodopa (L-DOPA_ given instead of dopamine in Parkinson’s disease?
Dopamine cannot cross the blood brain barrier so it must b given as a precursor
L-DOPA can can cross the BBB and is covered to dopamine in the basal ganglia
145
Why is carbidopa given alongside levodopa in Parkinson’s disease?
As levodopa is a precursor, some of it is converted to dopamine before it reaches the brain and basal ganglia
Dopamine present in the body can cause side effects e.g, vomiting, orthostatic hypotension
Carbidopa prevents levodopa from being converted to dopamine before it reaches the basal ganglia
146
What are the main side effects of levodopa?
Nausea and vomiting
Involuntary movements (dyskinesias)
Hallucinations, paranoia
Change in blood pressure e.g, orthostatic hypotension
147
Why can’t Parkinson’s disease be controlled with L-DOPA for a long term period?
After taking levodopa for 5+ years, patients can start to experiment on-off effects. Where the drug can work one second, and then not during other seconds
Patients are also more likely to experience dyskinesia side effects with long term use, as the threshold for dyskinesia is lowered
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How can the medication be changed for patients with Parkinson’s disease when they start to experience the on-off effects with levodopa?
Patients can take lower more frequent disease
Patients can take monoamine oxidase B inhibitors - these inhibit catabolism of dopamine in the brain and help to smooth out the end dose fluctuations causes dyskinesias e.g, rasagline
A dopamine receptor agonist can be added e.g, rotigotine
