CLASSIFICTION OF NEUROPATHY

1. Approach to peripheral
neuropathy

2. Typesof nerves and their function

3. Sensorysymptoms

4. Motor symptoms

5. Autonomic symptoms

6. Causes
• Systemic disorders
1. Endocrine – DM, hypothyroidism, acromegaly
2. Connective tissue – Sjogren, RA, SLE, MCTD, Vasculitis
3. Nutritional – B complex ( B1, niacin, B6, B12 ), vitamin E,
copper, B6 overdose
4. Inflammatory – AIDP, CIDP, Amyloidosis, Sarcoidosis,
hypereosinophilic syndrome, IBD, celiac disease
5. Metabolic – CLD, Uremia, Porphyria
6. Infective – Leprosy, HIV, Diphtheria, Lyme, Hep B & C
7. Malignancy – Paraneoplastic, Infiltration by leukemia &
lymphoma, Plasma cell disorders
8. Critical care neuropathy

7. Causes
• Toxic ( Drugs/toxin )
• Hereditary – CMT –M/C
• Environmental – Vibration induced, prolonged cold
exposure, hypoxemia
• Idiopathic – 46%. Most cases > 50 years. Progession –
slowly over months to years. Predominant sensory
symptoms. Proposed but unproven causes are HTn,
dyslipidemia, increased oxidative stress.

8. Drugs

9. T
oxins

11. Classification

12. Evaluation
• Mild symptoms with known underlying lesion like DM,
chemotherapy, alcohol abuse – No evaluation is required
• Feature warranting a full evaluation
Assymetry
Non length dependence
Motor predominance
Acute onset
Predominant autonomic involvement
Rapidly progressive symptoms
Sensory ataxia

13. Acute / abruptonset
• GBS
• Vasculitis
• Porphyria
• Infectious disease ( Lyme disease, diphtheria )
• Toxin / Drug – arsenic, thallium, chemotherapeutic agents,
depsone

14. Subacute/chronic
• CIDP
• DM
• Vasculitis
• HIV
• Vitamin B12
deficiency
• Copper deficiency
• Paraneoplastic
• Sjogren syndrome
• Toxin, Drug

15. Relapsingand remitting course
• CIDP
• Porphyri
a
• HNPP

16. General physical examination
Purpur
a
Vasculiti
s
Angiokeratom
a Fabry
disease
Hypopigmentatio
n Leprosy
Orange tonsil
Tangier’s
disease

17. General physical examination
1)Skin
hyperpigmentation
2)Clubbing
POEMS syndrome

18. General physical examination
Mess line
Arsenic or
thallium
intoxication

19. General physical examination
Retinitis pigmentosa,
Icthyosis
Refsum’s disease ( AR )
1) RP
2) PN
3) Cerebellar ataxia
4) Elevated CSF protein

20. General physical examination
• Thickened
nreves
Leprosy
Neurofibromatosi
s
Refsum disese
Amyloidosis
HMSN
DM
Sarcoidosis

21. General physical examination
• Purpura, Livodereticularis – Vasculitis, Cryoglobulinemia
• Angiokeratomas – Fabry’s disease
• Skin pigmentation – Leprosy, POEMS, adrenoleukodystrophy
• Icthyosis – Refsum’s Disease
• Mees’ line – Arsenic / Thallium Intoxication
• Alopecia – Thallium Poisoning, Hypothyroidism, SLE
• Maculoanaesthetic patches with thickened nerves - Leprosy
• Orange Tonsils – Tangier’s disease
• Pes cavus, high-arched feet and mutilation – Hereditary
neuropathy
• Macroglossia – Amyloidosis
• Chelosis/Glossitis – Multivitamin deficiency

22. Electrodiagnosis - Mononeuropathy
• Direct trauma
• Compression or entrapement
• Neoplastic compression or
infiltration

23. Electrodiagnosis – Mononeuritis multiplex
• Simultaneous / sequential damage to multiple noncontiguous
nerves.
Ischemia caused by systemic vasculitis. Painful (90%)
neuropathy progresses over weeks ). Can be patchy.
Sensory/sensorimotor. Lower
> upper. Distal > proximal. Constitutional symptoms present
in most of the patients.
Microangiopathy in DM – Diabetic amyotrophy

24. Electrodiagnosis – Mononeuritis multiplex
• Ischemic – Sickle cell, cholesterol emboli, atrial myxoma
• Inflammatory – Sarcoidosis, CIDP variants ( MADSAM,
MMN ), Eosinophilic disorders, A/W crohn’s, UC and
celiac disease
• Infectious – Leprosy, Lyme, Viral ( Hep B, Hep C, other viral
infection in immunocompromised patients )
• Genetic – HNPP, Familial amyloid neuropathy
• Neoplastic – Lymphoma, leukemia, paraneoplastic

25. Electrodiagnosis
Polyneuropathy
• Axonal vs demyelination
 Distal>Proximal vs
Distal=proximal
 LL>UL vs UL=LL
 Wasting vs weakness>wasting
 CMAP vs Latency, CV

27. Clue– Painful polyneuropathy
1. DM
2. Alcohol
3. Paraproteinemia
4. Vasculitis associated and connective tissue
associated
5. Amyloidosis ( familial, acquired )
6. Paraneoplastic sensory neuropathy ( Mainly
Lung )
7. Idiopathic small fibre neuropathy

28. Clue– Motor predominant
1. GBS
2. Porphyria
3. Lead
poisoning
4. Variant of
CIDP

29. Clue– Significant autonomic involvement
1. DM
2. GBS
3. Amyloidosis ( Familial, acquired )
4. Uremic
5. Porphyria ( descending neuropathy )
6. HIV related autonomic neuropathy
7. Hereditary sensory and autonomic
neuropathy
8. Vincristine

30. Clue- Neuropathies with cranialnerve
involvement
1. Diabetes mellitus
2. GBS
3. HIV/AIDS
4. Lyme disease
5. Sarcoidosis
6. Neoplastic invasion of skull base or
meninges
7. Diptheria
8. Friedrich’s ataxia

31. Clue– Drugswith demyelinating neuropathy
1. Amiodaron
e
2. Chloroquin
e
3. Suramin
4. Gold

34. Nerve biopsy
• Vasculitis, amyloid, leprosy, hereditary cause.
• Sural nerve.
• Occasional – superficial peroneal nerve. Biopsy of peroneous
brevis through same incision – Increases yield in vasculitis.

35. Skinbiopsy
• Small fibre neuropathy
• Very small piece of skin just proximal to ankle is removed.
• Special stains are applied - Qualitative assessment or by
careful counting to determine intraepidermal nerve fibre.

38. Thank
you

39. References
• Clinical Approach to Peripheral Neuropathy: Anatomic
Localization and Diagnostic Testing Adina R. Alport et al :
Continuum Lifelong Learning Neurol 2012;18(1):13–38.
• An Approach to the Evaluation of Peripheral
Neuropathies;Mark B. Bromberg; SEMINARS IN
NEUROLOGY/VOLUME 30, NUMBER 4 2010
• www.uptodate.com
• Harrison 20th edition