Neuro Flashcards
LL Neuro Schpiel
Today I examined ____ lower limb.
Pertinent findings were weakness in XXX with tone/reflexes/co-ordination/sensory findings of ____.
These findings are in keeping with an upper/lower/mixed motor neuron pattern consistent with a lesion at the XXXX.
My differentials are ….
Schpiel (Gait)
Today I was asked to examine ____ gait, which was ____.
Given these findings I went on to examine lower limb neuro, co-ordination/cerebellar/Parkinson’s.
My findings were ___ consistent with ____ and my differentials are _____.
-
Predominant sensory peripheral neuropathy causes
- Diabetes
- ETOH
- Hypothyroidism
- Uraemia
- Sarcoidosis
- Paraneoplastic
- B12 deficiency
- Infections, e.g., leprosy, HIV, Lyme disease
- Amyloidosis
- Drugs (isoniazid, metronidazole, hydralazine, disulfiram, chloroquine, pyridoxine, colchicine, flecanide).
Predominant motor peripheral neuropathy causes
- CIPD/GBS
- Drugs (Dapsone)
- Porphyria
- Lead
- Diptheria
Pes Cavus (inherited neuropathy) causes
- CMT
- Friedrich ataxia
- Muscular dystrophy
- Cerebral palsy
- Spinal cord tumour
- Poliomyelitis
- Syringomyelia
- HSP
Axonal loss signs
(Diabetes, ETOH, malignancy)
- Distal reflex loss
- Distal proprioception/vibration loss
Demyelinating loss signs
(HIV, drugs, MS)
- global areflexia
- decreased proprioception/vibration
- preserved pin-prick
Proximal limb weakness causes
Proximal myopathy:
- steroids, ETOH, statins
- diabetes, diabetic amyotrophy
- thyrotoxicosis
# IBM (quads) # Polymyositis/dermatomyositis # Mitochondrial myopathies # Hereditary causes - muscular dystrophies, fascioscapulohumeral dystrophy
Distal myopathy causes
- Myotonic dystrophy - facial and distal limb weakness, myotonia
- IBM (distal in UL)
Lower limb weakness differentials
# Mix of UMN & LMN with no sensory findings: - MND, cerebral palsy, lacunar infarct
UMN in upper and lower limbs, bilaterally:
- High cervical stenosis
- MS
- Arnold chiari malformation
LMN lesion in UL and UMN lesion in LL
- Syringomyelia
- Cervical lesions
Sensori-motor peripheral neuropathies:
- Inherited: CMT
- Acquired: Diabetes, CIDP
Neuromuscular disease:
- Myasthenia
- Lambert Eaton
Foot drop causes
Weak tibialis anterior
Common peroneal lesion - loss of eversion, sensory loss over lateral calf/dorsum of foot
L4/L5 root weakness - loss of eversion and inversion, expect dermatome sensory findings, may have hip abduction weakness
Bilateral peripheral neuropathy - all movements weak in glove/stocking sensory loss and areflexia.
UMN pattern:
- bilateral spastic paraparesis - spinal cord lesion, bilateral stroke, MND
- One leg weak - cortical infarct/lesion, Brown-Sequard
- Hemiparesis - Upper and lower limb weakness same side - ? stroke
Sciatic nerve lesions - loss of eversion/inversion and ankle jerk.
Anterior horn cell disease - polio
Other neuro spiel
- It is best to mention abnormalities as patterns rather than coming up with a diagnosis first up, e.g.,:
- UMN vs LMN or a combination
- Cerebellar dysfunction +/- other signs
- Peripheral neuropathy (sensory/motor)
You can then mention a list of possible diagnoses.
Neuro Cases
- Polyneuropathy - others (pure motor, sensorimotor - 21%
- Muscular dystrophy - myotonic - 14%
- CN lesions including pituitary tumours - 13%
- Multiple Sclerosis - 12%
- Myopathy/myositis - 12%
- Polyneuropathy - CMT - 7%
- MND - 7%
- Parkinson’s disease/PSP/Huntington’s
- Stroke - 7%
- Polyneuropathy - Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP)
Ability to stand on toes?
S1
Ability to stand on heels?
L4,5 –> foot drop
Romberg test
Steady with eyes open, unsteady with eyes closed:
- posterior column
- peripheral neuropathy
- vestibular function
Unsteady with eyes open & closed:
- cerebellar
*Unlikely to be related to cerebellar function in exam
Diplegic/paraparetic gait causes (5):
- SC lesion
- Cerebral palsy
- Bilateral strokes
- HSP
- MS
CP Lesion (foot drop)
CP CAN invert whereas L4/L5 or Sciatic lesions unable to invert.
CP, L4-5 or sciatic lesions CAN’T evert.
Ankle jerk preserved
Unilateral high stepping gait (unilateral foot drop) causes:
Distal weakness:
- L5 lesion
- CPN lesion
- Sciatic neuropathy - patient can walk on toes but not heel of affected side
Bilateral high stepping gait (bilateral foot drop) causes:
- Lumbosacral polyradiculopathy
- MND
- Distal polyneuropathy e.g., CMT (patient can’t walk on heels or toes), CIDP
- MD
High stepping gait of sensory neuropathy (sensory ataxic gait) causes:
Maybe wide-based, clumsy, slapping down of feet + Romberg’s:
- Peripheral sensory neuropathy
- Syphilis
- Subacute combined degeneration of the spinal cord
UL/LL Neuro *Don’t forget:
1) Scars, back, neck
2) Catheters
3) Peri-anal sensation, anal tone
Gerstmann’s syndrome (Dominant) - 4
1) Agraphia
2) Acalculia
3) Finger agnosia
4) Left-Right Confusion
Subcortical lesion:
- Internal capsule
- Basal Ganglia (Globus pallidus & Putamen)
- Thalamus
- Absent cortical signs
- Face, arm & leg equally affected
- Unusual movements (basal ganglia)
- Dense sensory loss (thalamus), maybe associated with hemiplegia
Brainstem lesion (5)
- Crossed hemiplegia, cranial nerve or cerebellar signs on side of brainstem affected opposite to hemiplegia
- Nystagmus horizontal, vertical
- INO (Internuclear ophthalmoplegia)
- Gaze palsy looking to side of lesion (pontine gaze centre controls gaze towards itself)
- Sensory findings: crossed sensory loss, 5th nerve (pain & temp) opposite to body sensory loss (spinothalamic)
Cortical signs (4)
- Aphasia
- visuospatial neglect
- gaze deviation
- visual field defects
*always absent in subcortical/lacunar strokes
Lacunar syndrome (5)
- Pure motor stroke/hemiparesis (most common lacunar syndrome: 33–50%)
- Ataxic hemiparesis (second most frequent lacunar syndrome)
- Dysarthria/clumsy hand (sometimes considered a variant of ataxic hemiparesis, but usually still is classified as a separate lacunar syndrome)
- Pure sensory stroke
- Mixed sensorimotor stroke
SC Lesion
- usually bilateral
- sparing of face, cranial nerves (rarely 5th nerve long tract affected)
- horner’s high spinal lesion, sympathetic chain down to T1, T2
- sensory level
- bladder, bowel dysfunction
- if unilateral look for Brown Sequard- hemitransection of the SC:
- ipsilateral spastic hemiparesis, loss of vibration & proprioception
- contralateral loss of temperature & pin-prick
CN 2 (4)
Optic Nerve:
1) Acuity (done first)
2) Fields
3) Pupil response
4) Fundi
Bi-temporal heminopsia (tunnel vision) causes:
1) Pituitary adenoma
2) Craniopharyngioma
3) Neoplastic - meningioma
4) Vascular origin is an aneurysm of the anterior communicating artery
CN 3 Palsy
Oculomotor
1) Ptosis
2) Inferolateral displacement of the ipsilateral eye (SR, IR. MR, IO)
3) Pupil
*PCOM Aneurysm - CTA
- MRI - stroke (ischemia), tumour, demyelination, GCA, infectious
Argyll Robinson Pupil
- Accommodates but does not react.
- bilateral small pupils that reduce in size on a near object (i.e., they accommodate), but do not constrict when exposed to bright light (i.e., they do not constrict when exposed to light).
- highly specific sign of neurosyphilis
RAPD (MG)
- observed during the swinging-flashlight test where upon the patient’s pupils dilate when a bright light is swung from the unaffected eye to the affected eye. The affected eye still senses the light and produces pupillary sphincter constriction to some degree, albeit reduced.
- most common cause is a lesion of the optic nerve (between the retina and the optic chiasm) due to glaucoma, or severe retinal disease, or due to multiple sclerosis.
Common causes of CN palsies (4)
1) Diabetes
2) Aneurysm
3) A vascular event
4) Mass lesion
Complex ophthalmoplegia (4)
1) Graves
2) MG
3) Mitochondrial myopathies - Chronic progressive external ophthalmoplegia
4) Occulopharyngeal l dystrophy
Stroke facial nerve
- spares forehead
- paralysis of contralateral lower face
Pseudobulbar palsy causes:
- Bilateral UMN Lesion
- Causes: MND, MS, multiple strokes, trauma, BS tumour
Bulbar palsy causes:
- Bilateral LMN Lesion
- Causes: MND, MG, GBS, Infarcts in medulla, Polio, Arnold Chiari malformation
Dysphasia types (4)
- Receptive - can’t comprehend what you’re saying and have a problem with repeating what you’re saying: Wernicke’s area - posterior section of the superior temporal gyrus, dominant cerebral hemisphere
- Expressive (motor aphasia): Brocca’s area - inferior frontal gyrus of the dominant hemisphere
- Nominal dysphasia: can’t reliably be localised
- Conductive: arcuate fascicles - deep white matter bundle connecting the posterior temporoparietal junction with the frontal cortex. *can’t repeat statements or name objects but can follow commands.
Dysarthria (3)
- Cerebellar (scanning speech: slow, jerky, slurred and often explosive, broken up into syllables
- UMN
- pyramidal (spastic) dysarthria: slow, laboured, patient trying to squeeze words out
- extrapyramidal e.g., PD: motonous, bradykinesia, muscular rigidity
- apraxic speech: pre-frontal motor dysfunction, difficulty constructing speech
- LMN
- nasal, flaccid (MG, MND with LMN signs, bulbar palsies)
- facial muscle weakness –> slurred speech
Posterior Column Lesions causes
1) Sub-acute combined degeneration of the cord - B12 deficiency - diet, malabsorption
2) Tabes dorsalis - syphilis
3) Friedrich’s taxia
4) Spinocerebellar ataxia
5) Paraneoplastic DRG-opathies
Syringomyelia
- ko’s the Spinothalamic tract
- spares the DCML
PD extra tests:
1) measure postural BP (autonomic dysfunction)
2) assess cognitive function (MMSE)
3) assess handwriting (micrographia)
Parkinsonism
1) BK with at least one of:
- tremor
- rigidity
- postural instability
PD
- Neurodegenerative disease caused by disruption of dopminergic neurotransmission in the basal ganglia. Loss of dopaminergic neurons in the substantia nigra.
CMT description
- Symmetrical distal motor and sensory neuropathy.
- Hyporeflexia
Bulbar palsy signs:
- Upper and lower facial weakness
- Palatal paralysis
- Wasted and flaccid tongue with prominent fasiculations
- Nasal quality speech
Pseudobulbar palsy signs:
- Emotional lability (laughing/crying)
- Stiff (spastic) tongue with no fasiculations
- *Brisk jaw reflex
UMN and LMN ddx
- MND (ALS)
- Syringomyelia
- Cervical myelopathy
Cerebellar lesion will result in IPSILATERAL signs.
Cerebellar lesion will result in IPSILATERAL signs.
Friedreich’s ataxia signs:
- Pes Cavus
- pryamidal and dorsal column signs in legs
- depressed ankle jerks
- extensor plantars
Cerebellar syndrome causes:
- Demyelination (MS)
- Alcohol cerebellar degeneration
- Posterior fossa SOL
- Brainstem lesions
- Friedreich’s ataxia
- Hypothyroidism
- Vitamin E deficiency
- Spinocerebellar degneration
- VHL syndrome
- MSA
Drugs:
- phenytoin
- Lithium
- Carbamazapine
- CTx agents
Myotonic dystrophy (trinucleotide repeat CTG expansion)
- myopathic/expressionless facies
- frontotemporal balding
- bilateral ptosis but can be unilateral
- distal wasting and weakness, i.e., distal myopathy
- high steppage gait
- overcome eye closure
- clench fist and open
Associated conditions with MD:
- diabetes
- cardiomyopathy - HF
- valvular heart disease - MVP
- arrhthymias - AF, SVT, VT
- conduction defects - PPM
- hypogonadism: gynaecomastia, testicular atrophy
- goitre
Peripheral neuropathy types:
- sensory (large fibre - DCML, small fibre - STT) - sensory loss in a stocking distribution
- motor (distal wasting and weakness, depressed reflexes)
- sensori-motor
Motor neuropathy signs:
- LMN pattern of weakness - wasting, weakness (distal to proximal, length dependent axonal degeneration), hyporeflexia and down-going plantars
Sensory neuropathy distribution:
- stocking distribution in the legs and glove distribution in the arms.
- distal-to-proximal axonal degneration.
Sensori-motor polyneuropathy causes:
- ETOH
- Diabetes
- Hypothyroidism
- Uraemia
- Sarcoidosis
- Vasculitis
- Paraneoplastic
- CIDP/GBS
- Hereditary motor and sensory neuropathies
Demyelinating polyneuropathy causes
- CIDP
- MM
- MGUS
- HMSN (CMT)
- HNPP
- Multifocal motor neuropathy
- HIV
Peripheral neuropathy Ix
- FBE
- ESR
- UEC
- LFT
- Glucose/HbA1c
- TFT
- B12, folate
- SPEP
- Autoimmune profile
- NCS
- CSF analysis
- Nerve biopsy
- Genetic testing
Common causes of CP injury:
External compression:
- short braces
- plaster cast
- tourniquets
- leg crossing
- prolonged pressure due to positioning during surgery
- schwanoma
Trauma:
- direct trauma to nerve
- fibula fracture
- following TKR
Causes of mononeuritis multiplex
Flaccid foot drop causes:
Muscle:
- MD
- Trauma
NMJ: MG
LMN: MND
LS plexus: pelvic pathology
Cauda equina: tumour
L5 nerve root: L4/5 disc prolapse
CP palsy
Sciatic nerve palsy: trauma, hip surgery
Friedreich’s ataxia (pes cavus (PN) plus cerebellar ataxia)) signs:
- cerebellar syndrome
- pes cavus
- pyramidal distribution of weakness
- depressed reflexes with extensor plantar responses
- peripheral neuropathy - loss of proprioception and vibration sense
High-arched palate causes:
- Friedrich’s ataxia
- Marfan’s syndrome
- Turner’s syndrome
- Tuberous sclerosis
Pyramidal weakness
- characteristic of UMN damage
LL: flexion is weaker than extension, ankle dorsiflexion, eversion.
UL: extension is weaker than flexion
DDx of depressed knee and ankle jerks with extensor plantar responses:
Combo of conditions:
- peripheral neuropathy and stroke
- peripheral neuropathy and cervical myelopathy
- cervical and lumbar spondylosis
- Subacute combined degeneration of the cord (B12 deficiency)
- Tabes dorsalis
- Lesion of the conus medullaris
- Friedreich’s ataxia
- MND
Multiple Sclerosis signs:
- eye (optic atrophy, RAPD)
- brainstem (INO, facial sensory loss, facial weakness)
- cerebellar (ataxia, dysarthria)
- pyramidal
- dorsal column signs.
Causes of spastic paraparesis:
- MS
- Cord compression - tumours
- Trauma
- MND
- Syringomyelia
- Anterior spinal artery occlusion
- Subacute combined degeneration of the cord
- Tabes Dorsalis
- Friedrich’s ataxia
- Cervical myelopathy
- HSP
- Transverse myelitis:
- bacterial infections: Lyme disease, mycoplasma, TB and syphilis
- Viral infections: HSV, VZV, CMV, EBV, HIV, HAV, influenza and echovirus
- Demyelination (MS and NMO)
- Radiation myelopathy
- Vasculitis
Cervical Myelopathy - most commonly caused by canal stenosis - degen change/trauma, tumours.
UL: absence of bicep and supinator reflexes coupled with DCML signs
LL: spastic paraparesis with DCML signs
Unilateral ptosis causes
- CN 3 palsy - Eye movements
- Horner’s syndrome *sympathetic chain - meiosis
- MG/LEMS
- Myopathy - myotonic dystrophy - usually bilateral
- Congenital
Bilateral ptosis causes
- MG
- Myotonic dystrophy
- Tabes dorsalis
- Bilateral Horner’s syndrome, e.g., syringomyelia
- Chronic progressive external ophthalmoplegia
- Miller Fisher Syndrome
Causes of central Horner’s syndrome (first order neurone):
- Demyelination
- BS or SC tumour
- BS or SC haemorrhage or infarction
- Syringomyelia
- Basal meningitis (syphilis, TB, carcinoma, lymphoma)
- Basal skull tumours
- Neck trauma
Causes of peripheral Horner’s syndrome (second order neurone):
- Pancoast tumour
- Cervical rib
- Neurofibromatosis
- Neck surgery
- CTS surgery
- Lymphadenopathy
- Aneurysms or dissection (aorta, subclavian or common carotid)
Causes of peripheral Horner’s syndrome (third order neurone):
- Internal carotid artery dissection
- Carotico-cavernous fistula
- Herpes Zoster
Four types of dysarthria
1) Cerebellar disease
2) MND (pseudobulbar or bulbar palsy)
3) PD
4) Syringomyelia (bulbar palsy)
Hemiparesis case add ons:
- Perform complete neuro exam (UL/LL/CN)
- Assess visual field defects (HH)
- Assess patient’s speech (particularly with R) hemiparesis-L) dominant hemisphere)
- Measure BP
- Assess pulse (AF)
- Auscultate for carotid bruits
- Check urinalysis (glycosuria)
- As if the patient is R) or L) handed
Causes of Hemiparesis:
- Stroke (ischaemic, haemorrhagic, thrombosis)
- Tumour
- Demyelination
- Abscess
- Post-ictal (Todd’s paresis)
- Functional
Cortical lesion signs
- aphasia
- neglect
- apraxia
- HH
- seizures
BS lesion signs:
- Cerebellar
- Eye movements/Horner’s
- Crossed signs: R) CN III or VII cranial never palsy plus L) hemiplegia)
PCA stroke
- Brainstem cerebellar signs as well as HH and memory problems
PCA supplies: occipital cortex, hippocampus and thalamus.
MCA lesion vs ACA lesion:
MCA lesion affects: unilateral UL and face
ACA lesion affects: unilateral LL
Causes of Chorea
Inherited:
- Huntington’s disease
- Wilson’s disease
- Spinocerebellar ataxia
Acquired:
- SLE
- PRV
- Thyrotoxicosis
- Hypo PTH with hypocalaemia
- Dopamine antagonists
- Stroke
Polio
- LMN signs (often unilateral) with the absence of sensory signs in a patient with hypoplastic limbs
Acute flaccid paralysis causes:
Infection:
- Viral
- Polio
- Enterovirus
- Coxsackie
- Japanese encephalitis
- Bacterial
- Botulism
- Diptheria
- Lyme disease
Neuropathy:
- GBS
- AIP
- Lead poisoning
Spinal disease
- Acute transverse myelitis
- Spinal cord compression
- Spinal cord infarction
Brainstem dysfunction signs:
- Ophthalmoplegia
- Conjugate gaze palsy
- Pupil involvement
- Nystagmus (esp vertical)
- Crossed signs, i.e., sensory and/or motor dysfunction affecting the limbs on one side and the face/bulbar muscles on the other side
- Ataxia
- Bilateral pyramidal signs, e.g., extensor plantars or quadriparesis
- Respiratory or autonomic involvement
VSIP
- Vascular
- SOL
- Inflammatory
- Paraneoplastic
Lateral medullar syndrome (4) - Posterior inferior cerebellar artery - secondary to vertebral artery stenosis or dissection.
- Ipsilateral Horner’s syndrome
- Ipsilateral cerebellar signs
- Ipsilateral V (STT), IX, X and X nerve signs
- Contralateral STT (below the lesion)
- Sensory of V
Power scale:
0 - no contraction
1 - flicker or trace of contraction
2 - active movement with gravity eliminated
3 - active movement against gravity
4 - active movement against gravity and resistance
5 - normal power
UMN Signs (3)
- Hyper-reflexia
- Spasticity
- Up-going plantar reflexes
LMN Signs (4)
- Hyporeflexia
- Fasiculations
- Decreased tone/flaccid
- Atrophy
Horner’s signs (3)
- Ptosis
- Meiosis
- Anhidrosis
Binocular diplopia ddx (6)
does it go away with EITHER eye?
- supranuclear
- nuclear
- infranuclear
- nerve
- muscle
- NMJ
Monocular diplopia ddx (4)
does it go away with one eye?
- refractive error
- corneal disease
- cataract
- dry eye
Myopathy (6)
- Usually proximal weakness
- Usually no sensory deficit
- Reflexes preserved until late
- Fasiculations absent
- Contractures present
- May be associated with myocardial dysfunction or muscle tenderness
Neuropathy (6)
- Distal weakness
- Concomitant sensory symptoms + signs
- Reflexes lost early
- +/- fasiculations
- No contractures
- Not associated with myocardial dysfunction nor muscle tenderness
NCS - Axonal pattern
- Decreased amplitude
NCS - Demyelination
- Decreased conduction velocity
- Increased latency
Horizontal diplopia
- CN 3 or 6
*due to disease of the medial or lateral rectus muscle, the neuromuscular junction, or the nerves supplying these muscles
Vertical diplopia
- CN 4
Causes: congenital, microvascular disease, or trauma
Diagonal diplopia
- CN 3 or 4
*reflects dysfunction of both vertical and horizontal muscles, suggests dysfunction of the oculomotor nerve (involving some combination of the inferior rectus, superior rectus, and inferior oblique muscles).
PRES (reversible posterior leukoencephalopathy syndrome)
- Headache, confusion, visual symptoms, seizures
Multiple sclerosis
- Periventricular
- Cortical/juxtacortical
- Infratentorial
- Spinal cord
McDonald’s criteria
- Demonstration of CNS lesions in both space (PV, JC, IF, SC) AND time.
LEMS
- SCC lung Cx
- *EMG: incremental response
- Anti-voltage gated calcium channel
MG
- Anti AcHr-Ab, MUSK ab
- Tensilon test
- EMG - jitter/decrementation
- CT Thorax - thymoma
CN 4
- SO *Controls intorsion of the eye in down-gaze
Where is the lesion? (8)
1) Cortical - vision/speech, neglect
2) Subcortical - lacunar - pure motor, sensory
3) Brainstem - Opthalmoplegia has to be BS
4) SC - sensory level + UMN until L-S spine
5) Nerve root - brachial plexus
6) Peripheral nerve - dermatome - radiculopathy, plexopathy
7) Muscle - myopathy
8) NMJ
Stroke (6)
1) Location
2) ? Cause - carotid/thromboembolic disease/small vessel disease (older - T2DM, HTN, Hcol, smoker)
3) Loop, Holter, TTE - ? PFO closure (younger)
4) Rx - aspirin/clopidogrel
5) Impact on function from stroke
6) Return back to work and Driving Ax
Medial Medullary Syndrome
- Ipsilateral INO
- Contralateral DCML
- Contralareral hemiparesis
- Ipsilatreral 3, 4, 6 and 12
Anterior spinal atery
7 Classical features of Parkinsonian Gait
- Stooped and rigid posture
- Difficulty with initiation
- Narrow-based (not a pathological feature)
- Shuffling and festinating
- Reduced arm swing
- Clock-face turning
- Freezing of gait
Spasticity
- Velocity and degree dependent
Rigidity
- Velocity and degree independent
Long term issues of MS (9)
- Pain (spasticity)
- Immobility (ataxia)
- Numbness
- Continence - urinary retention, self-IDC, constipation
- Ataxia
- Fatigue
- Cognitive issues
- Employment
- QOL
Ophthalmoplegia possibilities (6):
- CN Palsy - Diabetes, Aneurysm, HIV, syphilis
- Graves
- MS
- MG
- Mitochondrial - MELAS (Mitochondrial encephalomyopathy, lactic acidosis and stroke-like episode)
- Miller-Fisher Variant CIDP
Miller-Fisher Variant CIDP (3)
- Ophthalmoplegia
- Ataxia
- Areflexia
- Anti-GM1, GD3, GQ1b
Stroke causes (5)
- Cardio-embolic (20%)
- Large artery disease (20%)
- Subcortical (25%)
- Cryptogenic (30%(
- Vasculitis, genetic, VST (5%)
MS Sx Rx options (4):
- Motor disability: gait aids, PT, OT, spasticity, NDIS
- Bladder: anti-cholinergics, mirabegron, botox, continence clinic
- Pain: neuropathic, spasticity, botx, baclofen, CBD-THC
- Mood/anxiety Rx
