Teaching Handout – Neurology – Peripheral Nervious System
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Things worth knowing for finals in black. Thorough and optional things in grey. For interest sake only
Examination of myotomes
Shoulder abduction (deltoid)
Elbow flexion (biceps/brachioradialis)
Elbow extension (triceps)
Wrist Extension (ECRL)
Finger Extension (long/short extensors)
Finger abduction (dorsal interossei)
Hip flexion (iliopsoas)
Knee Extension (quadriceps)
Knee Flexion (hamstrings)
Ankle DF (tibialis anterior)
Ankle PF (gastrocnemius/soleus)
C5
C6
C7
C7
C8
T1
L1/2
L3/4
L5/S1
L4/5
S1
Arms up, keep them up
Pull me towards you / fist to your shoulder
Push me away
Arms out, cock your wrists back, keep them up
Fingers out strong
Push against my finger
Lift your leg up, keep it up
Kick your foot to the ceiling
Knees bent, heel towards your bottom
Toes up to the ceiling
Push down on my hand
This is a myotomal examination. Should your initial inspection/tone/myotomal power testing suggest a possible
peripheral nerve lesion, only then it would be appropriate to go on to assess individual nerves ( median, ulnar,
radial, common peroneal, tibial etc) otherwise move on.
1. Immobilise the joint your are testing
2. Compare same movement on both sides
3. Ideally test using a muscle group of similar power to that you are testing
Muscle power should be tested as power at a static position, resisting movement (rather than range of
movement). Instructions to the patient should focus on achieving this. Hence, ‘cock your wrists back, don’t let me
push them down’ is a better test than ‘push your wrists back against my hand’ – for some reason, people are
able to ‘resist’ more strongly and reliably than producing an active movement. (Though some movements are
rather difficult to describe in this way). Try it yourself.
In testing sensation, I have been taught (and found) that the most sensitive test of nerve dysfunction is an
alteration, rather than absence of sensation. When asking patients whether they can feel the cotton wool/pin,
they will often say ‘yes’, but not tell you that it does feel different. Hence ‘same or different’ for cotton wool and
‘sharp or dull’ for pinprick. You get both the positive confirmation that they have felt the stimulus, and the added
information of it’s quality.
When testing pinprick, I usually preface with the instruction ‘this is a pin, it feels sharp but won’t break the skin’.
Does it feel sharp?
Patterns of Neurological Compromise
Descriptive
LMN UMN
Bilateral Unilateral
Symmetrical Asymmetrical
Distal Proximal
Motor Sensory Mixed
Deficit
Level
Myopathy
NMJ
Peripheral Neuropathy
Peripheral Merve lesion (s)
Plexopathy
Radiculopathy
Cauda equina
Spinal cord lesion/Myelopathy
Brainstem lesion
Cortical lesion
Patterns of deficit
Corticospinal – UMN, pyramidal motor deficit
Anterior Horn Cells – LMN motor deficit (eg. polio)
Dorsal column – light touch, vibration, proprioception
Spinothalamic – pain, temperature
Peripheral nerves – sensorimotor deficit
Peripheral Neuropathy
Common
Metabolic
Paraneoplastic
Infiltrative
Drug-Induced
Mononeuropathy
External Compression
Internal Compression
Intrinsic lesion
Diabetes, B12 Deficiency
Diabetes, B12/folate, alcohol
Lung, Ovarian, lymphoma, ENT/Adenocarcinoma
Amyloid, Sarcoid
Amiodarone, Chemotherapy- Vinca-Alkaloids(vincristine), Velcade (Bortezolemib)
Trauma, prolonged compression (eg. Coma)
Entrapment (eg. Carpal tunnel), tumors
Inflammation (usually part of a polyneuropathy/ MNM
Vasculitic (SLE, Rheumatoid, ANCA associated)
infiltrative (Amyloid, Sarcoid)
Failure to repair (metabolic) and minor compression
- Diabetic microvascular disease, alcohol, B12
Common Peroneal Nerve Palsy
Causes
Trauma/Compression at fibula (crossing legs!)
Acute mononeuritis - Diabetes, Vasculitis
Predisposition to pressure palsy/neuropathy
- Diabetes, B12 deficiency, Alcohol, Hypothyroidism
Inspector Morse with his foot drop - most common lower limb nerve mononeuropathy
THINK PERONEAL COMPARTMENT (which is lateral calf)
Motor – weakness of dorsiflexion, and eversion and toe extension but *sparing of inversion*
Sensory changes – lateral calf and dorsum
Ankle jerk preserved (S1 via tibial nerve)
Differentials of foot drop
L4L5 radiculopathy – but would involve medial sensory calf sensory change
Sciatic Nerve (more extensive motor/sensory deficit)
Peripheral neuropathy - glove/stocking sensory loss
Mononeuritis Multiplex
Common
Diabetes
Vasculitis
Systematic
Infection
Infarction
Inflammation
Infiltration
Iatrogenic
Neoplastic
Congenital
Metabolic
Hormonal
Lyme, Hep B, Hep C, HIV
-Vasculitic - SLE, Rhematoid, ANCA associated
Amyloid, Sarcoid
Amiodarone, Chemotherapy (vincristine, thalidomide), Ethambutol
Lymphoma, myeloma
Charcot Marie Tooth
Diabetes, B12, CKD, liver disease
Hypothyroidism
Multifocal Motor Neuropathy
Is
Acquired inflammatory demyelinating polyneuropathy affecting the motor axons.
Produces a LMN bilateral asymmetrical predominantly distal pure motor neuropathy, usually involving the upper limbs.
Muscle wasting and fasciculation are often absent.
(In finals if you (are unlucky enough to) get this, the only thing you will be expected to do is localise this to a LMN
lesion affecting the motor system, and suggest a few semi-sensible LMN pathologies and initial investigations)
Management
Full Hx and Ex to establish diagnosis and effect of the condition. Investigations include looking for other causes, using
nerve conduction studies, MR imaging of the cord and nerve roots, and blood tests for condition such as diabetes and
the vasculitides. LP may show oligoclonal bands in the CSF and there is an association with anti-GM1 IgM
Treatment is multidisciplinary. (OT, physio, social/community/group support) Medical treatment involves
immunomodulation with regular IVIG infusions.
Differentials:
Amyotrophic Lateral Sclerosis (ALS/Motor Neurone Disease – but this has UMN signs)
Plexopathy/Diabetic Amyotrophy
Causes of Mixed UMN and LMN
signs
General
Motor Neurone Disease
Two pathologies
Look for Bulbar signs
(eg. Cord compression and peripheral nerve compression)
Syringomelia (expanding central
canal, usually cervical)
Early spinothalamic tract pain/loss of pinprick. LMN wasting and weakness of
small muscles from early ventral root compression. UMN spasticity from
corticospinal tract involvement late in disease course
Absent ankle jerks and upgoing plantars
Caused by damage to corticospinal tracts (plantars) and peripheral nerve damage (loss of ankle jerks)
Subacute Combined Degeneration of Cord
2 pathologies
Taboparesis 2’ neurosyphilis
Friedrichs ataxia
Look for autoimmune disease, dementia
Eg. Cord compression + diabetic neuropathy
Charcot joints, Argyll Robertson pupils
Skeletal deformity, cerebellar signs
Causes of UMN signs
General
Cord / Myelopathy
Intracranial
Compression:
Disc
Trauma
Tumor (primary or metastatic)
Degeneration (spondylosis)/ (AA subluxation in Rheumatoid)
Abscess
Inflammation – multiple sclerosis
Infarction - anterior spinal artery infarction
Mass lesion
Tumor - Primary (meningioma, astrocytoma, glioblastoma)
Tumor - Secondary
Infarction – stroke – haemorrhagic or ischaemic
Inflammation – MS
Infection – encephalitis, meningitis
Autoimmune – autoimmune/paraneoplastic encephalopathies
Degeneration – frontotemporal dementias, other
Hydrocephalus
Tumors that metastasise to bone
5 ‘B’s - most rubbish mnemonic ever
Breast
Bronchus
Bidney (kidney)
Byroid (thyroid)
Brostate (prostate)