Neurology Flashcards
Types of increased tone
Spasticity and Rigidity
Difference between spasticity and rigidity
In spasticity resistance is different in different directions and is velocity dependent
In rigidity resistance isn’t direction dependent
Spasticity associated with
Upper Motor Neuron Lesions
Rigidity associated with
Basal Ganglia
Grading Power
0 - no muscle contraction seen
1 - flicker of contraction seen, not enough to move the joint
2 - muscle can move if gravity is eliminated
3 - muscle can move the joint with full range but without any resistance
4 - muscle can move the joint against partial resistance
5 - the muscle can move the joint against full resistance
Power 2 =
Slight movement with gravity eliminated
Usually a movement parallel to the floor
Power 3 =
Movement against gravity
Power 4 =
Movement against resistance
Management of Trigeminal Neuralgia
Carbamazepine
Preventative Medications in MS (3)
Natalizumab
Alemtuzumab
Ocrelizumab
Prophylaxis of Cluster Headaches
Verapamil
Management of Cluster Headaches (Acute)
High flow oxygen
S/C Sumatriptan
Provocation Procedures in EEG (2)
- Hyperventilation
= vigorous breathing results in a transient respiratory alkalosis, causes the constriction of small cerebral blood vessels
Decreases oxygen supply to the brain - Photic Stimulation
= stimulation with flashes of light to elicit visual responses in the occipital region
Dysphagia from a neurological cause
More likely to be dysphagia to liquids then solids
Examination Findings in Motor Neurone Disease
Finding pattern
Fasciculation and brisk reflexes
Pout reflex
Weakness of shoulder abduction
See mixed pattern - combination of UMN and LMN signs. See a LACK of sensory symptoms
Bulbar Palsy =
= signs/symptoms occurring due to an impairment of CN IX-XII due to lower motor neurone
Affects muscles of mastication, facial muscles and tongue
Pseudobulbar Palsy =
= inability to control facial movements, caused by damage to the corticobulbar pathways
= UMN lesion
Corticobulbar Pathways are
The UMN course from the cerebral cortex to the nuclei
Investigation of MND
Need MRI, neurophysiology and CK
Usually trying to exclude mimics/other differentials
Drug management in MND
Riluzole - prolongs survival
Management in MND
SALT and OT
Non-invasive ventilatory support e.g. BiPAP
PEG feeding can be used as long as there isn’t significant bulbar dysfunction
Investigation of choice in suspected SAH
Non-contrast CT, under 6 hours of first presentation
Contrast isn’t always of benefit
Preventative medications that can be used in migraine
Propranolol
Topiramate
Amitriptyline
Candesartan
Medication to ease vomiting in migraine
Prochloperazine
Eye Examination Findings in MS (3)
Pale optic disc on affected side
Relative afferent pupillary defect on affected side
Reduced visual acuity on affected side
Examination Findings in MS (5)
Pin and temperature loss on side of weakness Spasticity Weakness of shoulder abduction Brisk reflexes Extensor plantars
Presentation of GBS (2)
Distal weakness and sensory disturbance
May see areflexia/diminished reflexes
Monitoring Requirements in GBS
Vital signs
FVC - GBS can produce a restrictive lung problem
What antibodies can be seen in GBS?
Anti-ganglioside antibodies
Seen in up to 60% of GBS cases
Management of severe GBS
IV immunoglobulin
Plasma exchange
What is CADASIL?
Presentation?
Genetics?
Hereditary stroke disorder
Presentation = migraine with aura, subcortical TIA, progresses to vascular dementia
Genetics: mutation of Notch 3 on Ch 19
Stiff Person Syndrome
Presentation
Investigation
= stiffness of axial muscles and superimposed painful spasms
Ix: EMG evidence of continuous motor unit activity, anti-GAD antibodies (tens of thousands)
Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)
= neurological disorder characterised by progressive weakness and impaired sensory function
Often seeen as the chronic progression of GBS
CIDP
Pathophysiology
Management
Path: damage to the myelin sheath via an unknown autoimmune mechanism
Mx: corticosteroids and IV immunoglobulin
Physiotherapy may improve muscle strength
What are the Parkinson Plus Syndromes?
Multiple System Atrophy
Dementia with Lewy Bodies
Progressive Supranuclear Palsy
Corticobasal Degeneration
What areas of the brain are affected in PSP?
Basal ganglia
Brainstem (especially the midbrain)
Cortex (frontal lobes, limbic system)
Presentation of PSP (5)
Loss of balance Slowing of movement Impairment of vertical gaze Dementia Pseudobulbar palsy Procerus Sign = characteristic furrowing of the forehead with frowning expression and wide eyed stare
Presentation of Pseudobulbar Palsy
= UMN lesion of CN IX-XII Slow indistinct speech Dysphagia Brisk jaw jerk UMN signs in the limbs
MRI findings in PSP
Atrophy in the midbrain
Differentiating between Parkinson’s and PSP
Both have slowed movements and gait difficulty
Tremor common in Parkinsons, rare in PSP
Abnormal eye movements in PSP, normal in Parkinsons
PSP also has a poor response to levodopa
Presentation of Multiple System Atrophy (4)
Autonomic Dysfunction e.g. orthostatic hypotension, impotence, dry mouth, urinary retention/incontinence
Tremors
Slow Movement
Muscle Rigidity
Types of MSA
MSA-P - parkinsonian features dominate
MSA-C - cerebellar features dominate
Neurons degenerated in MSA (3)
Basal ganglia
Inferior olivary nucleus
Cerebellum
Management of MSA
Little levodopa response
Fludrocortisone is useful to prevent orthostatic hypotension
Definitive way to diagnose corticobasal degeneration
Neuropathology Examination
Presentation of corticobasal degeneration (4)
Parkinsonism
Alien Hand Syndrome = unable to control hand movements, feel that the hand is foreign
Apraxia
Aphasia
What are Lewy Bodies?
A-synuclein cytoplasmic inclusions, eosinophillic
Presentation of Dementia with Lewy Bodies (4)
Fluctuating cognition
Impairments in attention + executive funciton
REM sleep disorder
Visual hallucinations
Investigation of Dementia with Lewy Bodies
SPECT imaging is best
Need to avoid using haloperidol in
Dementia with Lewy Bodies
Can cause irreversible Parkinsonism
Management of Dementia with Lewy Bodies
Acetylcholinesterase inhibitors
e.g. donsepil, rivastigmine
Features of Parkinsonism (4)
Tremor
Bradykinesia
Rigidity
Postural Instability
Gait seen in PD
Stooping, shuffling gait
Non-Motor Features of PD (3)
Anosmia
Depression
REM sleep disorder
Investigation of PD
Usually clinical diagnosis
MRI often normal
SPECT imaging can be helpful
Management of PD
Levodopa
May use MAO-B inhibitor or dopamine agonist
Complication of PD/not taking PD medication
Neuroleptic Malignant Syndrome
= high fever, confusion, rigidity, sweating, increased heart rate
Can lead to rhabdomyolysis, high K+ and seizures
Which drugs block sodium channel influxes in the presynaptic neuron?
Carbamazepine
Lamotrigine
Phenytoin
Which drugs block calcium channel influxes in the presynaptic neuron?
Gabapentin
Pregabalin
Which anti-epileptic blocks neurotransmitter release?
Levetiracetam
Todd’s Paralysis
Post-ictal temporary paralysis
Types of Posturing
Decerebrate
Decorticate
Management of Partial Seizures
Lamotrigine
Carbamazepine
Presentation of Partial Seizures (Motor Fx)
Jerking, posturing, vocalisations
Difference between simple and complex partial seizures
Simple = no impairment of consciousness, no post-ictal symptoms Complex = impairment of consciousness, may see post-ictal confusion
Where do complex partial seizures most often originate from?
Temporal lobe
Presentation and Investigation of Absence Seizure
< 10 second pauses
See generalised spike wave abnormalities
Management of Absence Seizures
Ethosuximide or Sodium Valproate
Presentation of Tonic Clonic Seizures (3)
Loss of consciousness
Limb stiffening then limb jerking (tonic-clonic)
Post-ictal confusion (15 mins - 1 hour)
Management of Tonic Clonic Seizures
Sodium valproate
Can offer lamotrigine if SV inappropriate
Carbamazepine can make what types of seizure worse?
Myoclonic
Atonic
Presentation of Myoclonic Seizures (2)
Sudden jerk of limbs, face and trunk
May see violently disobedient limb
Management of Myoclonic Seizures
Sodium Valproate
OR Levetiracetam OR Topiramate
Presentation of Atonic Seizures (2)
Sudden loss of muscle tone results in fall
No loss of consciousness
Precipitants of Atonic Seizures (4)
Hyponatraemia
Infection
Head trauma
Withdrawal of anti-convulsants
Initial drug of choice for Status Epilepticus
Lorazepam 4mg IV
Difference between epileptic seizures and functional seizures
Epileptic - eyes are open: won’t be able to resist
Functional - eyes shut
Management of Spasticity in MS (2)
Baclofen
Gabapentin
Investigation of GBS
Use LP
Normal except high protein
Extradural bleed VS subdural bleed difference on CT
Extradural = limited by the sutures Subdural = not limited
Acute VS chronic subdural bleed
Acute = bright Chronic = hypodense/dark
Management of MS
Pyridostigmine
The -stigmines are ACh-esterase inhibitors
Investigation of choice in MS or demyelinating neuropathy
MRI with contrast
Contrast helps to identify areas of inflammation
Meralgia parasthetica =
= entrapment of the lateral femoral cutaneous nerve, results in sensory changes
Blood Tests Findings in Neuroleptic Malignant Syndrome (2)
Raised CK
Raised WBCs
= acute phase response
Lacunar infarct =
= can be a pure motor stroke, if so affecting the INTERNAL CAPSULE
Arteries e.g. lenticulostriate
Bulbar VS Pseudobulbar Palsy
Bulbar = LMN lesion of CN IX-XII Pseudobulbar = UMN lesion of CN IX-XII: more common
