Case

1
Case2 A 39 y/o male with HIV and progressive
numbness in feet

• The pt presented with 5-months h/o progressive
  numbness and pain in his feet followed by
  difficulty to walk, uses a cane. During work-up
  he was diagnosed with HIV.
• He, also, complained of weakness in his hands,
  and inability to button clothes or use pen or
  pencil very well.
• He denied any fever/chill/wt-loss or any other
  complaint.

2
Case2 HP

• PMH h/o syphilis 6-months ago, s/p penicillin
  injection x 3 doses.
• Soc Hx tobacco 1 ppd, beer 40 oz/day, quit
  coccaine 1-year ago, heterosexual, a total of 16
  sexual partners.
• Allergy NKDA
• Vitals T-97.4, P- 76, R-20, BP-132/65

3
Case2 HP

• PE Gen- no acute distress.
• HEENT/CV/Lung/abdomen- unremarkable
• Neuro- AO x 3 4/5 strength in bilateral biceps
  and triceps 4/5 strength in quadriceps and
  hamstrings DTR- absent decreased vibratory
  sensation in LE below calf finger to nose, rapid
  alternating movements, heel-knee-shin movements
  were slow but no ataxia.
• Gait- wide-based but the pt was able to ambulate
  without a cane.
• CD4- 210, VL- 89,000

4
Case2 Labs

• RPR- positive (12).
• Wbc- 2.9, Hg- 11.4, plt-127, Cr- 0.9
• CXR- normal
• Anti-HBc neg, anti-HBs neg, anti-HCB neg,
  anti-HAV neg, Toxo IgG neg, CMV IgG positive,
  G6PD 217.

5
Case2 Disease course

• The EMG and NCT showed severe diffuse slowing of
  conduction velocity throughout absent sural and
  ulnar potentials, and prolonged F waves.
• Suggestive of chronic inflammatory demyelinating
  polyneuropathy (CIDP).

6
Case2 Disease course

• The pt received IVIG for 5-days with significant
  improvement of symptoms for 4-weeks, then started
  to regain them.
• CD4- 170, VL-29,806
• Not taking PCP prophylaxis, missing appointments.

7
Topics of discussion

• 1. HIV-associated neuropathies.
• 2. Clinical features of HIV-associated sensory
  neuropathies.
• Treatment of HIV-associated sensory neuropathies.

8
HIV-associated neuropathies

• Peripheral neuropathy has emerged as the most
  common neurological complication of HIV infection
  (Arch Neurol 200158 1561 J Peri Nerve Syst
  200168)
• They are classified according to (1) the timing
  of their appearance during HIV infection, (2)
  their etiology, and (3) whether they are axonal
  or demyelinating.

9
HIV-associated neuropathies

• A. Distal symmetrical polyneuropathies (DSP)-
  distal sensory loss and neuropathic pain, caused
  by immune dysfunction, macrophage-mediated axonal
  injury.
• B. Mononeuropathy multiplex (MM)- multiple,
  asymmetric mononeuropathies, usually painful. It
  can occur both early in infection, by vasculitic
  mechanism, and in advanced stage by opportunistic
  pathogens, such as CMV and varicella zoster
  virus. May also occur 2ndary to hepatitis B and C
  viruses, when associated with cryoglobulinemia.

10
HIV-associated neuropathies

• C. Acute and chronic inflammatory demyelinating
  polyradiculoneuropathies (AIDP and CIDP) occur in
  the early stages of HIV, probably represent
  autoimmune phenomena (Ann Neurol 19872132). CSF
  studies show lymphocytic pleocytosis and elevated
  protein.
• Manifest with motor and sensory signs, nerve
  conduction studies show demyelinating features.

11
HIV-associated neuropathies

• D. Progressive polyradiculopathy- lumbosacral
  pain, saddle anesthesia, rapidly progressive
  flaccid paraparesis. May be caused by CMV
  infection (necrotizing neuropathy) or VZV
  infection (schwann cell and endothelial cell
  infection).

12
HIV-associated neuropathies

• E. Diffuse infiltrative lymphocytosis syndrome
  sensorimotor, painful, distal sensory neuropathy.
  Caused by CD8 lymphocytic infiltration in
  peripheral nerves associated with high viral
  loads.

13
HIV-associated sensory neuropathies (HIV-SN)

• HIV-SN is the most prevalent neuropathy.
• Clinical features The pain is the dominant
  symptom, typically bilateral, of gradual onset,
  described as aching, painful numbness, or
  burning (Neurology 198838794).
• The pain is usually most severe on the soles of
  the feet, and is typically worse at night.
• Typically, the dysesthesias ascend up the lower
  extremities over months, may begin to involve the
  fingertips at around the same time as they reach
  the mid-leg level.
• Weakness is a rare symptom.

14
Clinical features of HIV-SN

• Examination usually reveals absent or reduced
  ankle reflexes in addition to distal sensory
  loss.
• Electrophysiological studies usually show an
  axonal, sensory, polyneuropathy.

15
Treatment of HIV-SN

• Primarily symptomatic.
• ART have been demonstrated to improve thermal
  thresholds in those who show virological
  responses (Neurology 2000542120).
• Pain modifying agents Some degree of pain relief
  has been reported in small trials of both topical
  5 lidocaine gel and the anticonvulsant drug
  gabapentin (AIDS 1999131589 Eur J Neurol
  2001871).

16
Treatment of HIV-SN

• In placebo-controlled trials of pain modifying
  therapies, most agents (including amitryptiline,
  mexilitine, topical capsaicin and acupuncture)
  shown to be either ineffective or not more
  effective than placebo in relieving pain (JAMA
  1998280 1590 Neurology 1998511682).

17
Treatment of HIV-SN

• In randomized, placebo-controlled trials the only
  therapies shown to be effective are lamotrigine
  and recombinant human nerve growth factor
  (Neurology 2000542115 Neurology 2000541080).