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10 e
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27 Co
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 In
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Fe D
br ise
ua as
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27 Co
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8, re
20 nc
HIV clades worldwide

10 e
Neurological Manifestations of HIV infection
Directly due to HIV

10 e
20 nc

8, re
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27 Co
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Fe D
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20 nc
8, re
encephalitis

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27 Co
Clinical Psycho-motor Delirium, Focal signs

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Features slowing seizures,

br ise
brainstem signs

Fe D
Course months Days-weeks Weeks-months

n s
, o ou
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op fe
CD4 count <500 hi in <100 <100
Et uro
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atrophy/WM lesions
s io
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hyperintensities
Ad ter

CSF Non-specific PCR+90% PCR+80%

In
 10 e
20 nc
8, re
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27 Co
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20 nc
8, re
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27 Co
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Fe D
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Ab n
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Ad ter
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27 Co
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27 Co
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8, re
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PET scan

10 e
 Mild
In
Ad ter

Dementia
di nat
s io
Ab n
ab al N
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a, e
Et uro
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, o ou
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Fe D
br ise
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27 Co
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8, re
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20 nc
10 e
HIV associated Neurocognitive
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10 e
20 nc
8, re
Subacute

-2 nfe
27 Co
High HIV RNA, no HAART or

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ia cti
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op fe
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 In
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27 Co
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patients (Simioni et al. 2009)
Prevalence of HAND in aviremic
 In
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10 e
20 nc
8, re
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:%,-)+)$#/'/9%(7/1)-0%-1(V26:7W

10 e
20 nc
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8, re
-2 nfe
27 Co
CD4 <200

ry e
ua as
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Fe D
n s
, o ou
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op fe
hi in
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di nat
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ApoE4
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TNF receptor polymorphisms
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10 e
20 nc
8, re
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27 Co
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Fe D
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In

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 In
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8, re
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10 e
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27 Co
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, o ou
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gp120 R"#X/(%'(".I=(PZZ]
Jones et al., 2000; Kruman et al., 1998
 HIVE
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a, e
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HIV no encephalitis

Jones, Bell and Nath (unpublished)

ia cti
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27 Co
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8, re
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 In
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ua as
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27 Co
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8, re
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10 e
Cellular toxins
 Principles of Therapy for
HIV CNS infection

10 e
20 nc
8, re
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27 Co
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HIV RNA

ua as
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, o ou
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Ab n
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10 e
20 nc
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8, re
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:RS3

27 Co
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ua as
stavudine (D4T)

br ise
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n s
, o ou
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abacavir (ABV)
op fe
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a, e
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efavirenz (EFV)
Ab n
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di nat

nevirapine (NVP)
Ad ter
In

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indinavir (IDV)
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10 e
20 nc
8, re
-2 nfe
27 Co
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ry e
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Fe D
n s
, o ou
organic transporters

ia cti
op fe
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a, e
ab al N

No effect post viral integration

Ab n
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di nat

viral reservoirs spared

Ad ter
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early viral proteins still produced

 8>&B')&"'/+(S;%-"B>

10 e
20 nc
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8, re
-2 nfe
27 Co
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ry e
ua as
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gabapentin or topiramate.

, o ou
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op fe
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hi in
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inhibitors
a, e
ab al N

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Ab n
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agonists
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 In
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8, re
20 nc
10 e
 In
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ab al N
a, e
Et uro
hi in
op fe
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, o ou
n s
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br ise
ua as
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27 Co
-2 nfe
8, re
HIV infection and

20 nc
10 e
Cerebellar degeneration
(Tagliati et al., Neurology 1998;50:244-51)
 In
Ad ter
di nat
s io
Ab n
ab al N
a, e
Et uro
hi in
op fe
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n s
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br ise
ua as
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27 Co
-2 nfe
HIV+ Cocaine

8, re
20 nc
10 e
(Meltzer et al., AJNR 1998;19:83-9)
8yr old with congenital HIV infection with
microcephaly and developmental delay

10 e
20 nc
developed sudden onset of hemiparesis. CT

8, re
-2 nfe
showed subarachanoid hemorrhage

27 Co
ry e
ua as
br ise
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n s
, o ou
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hi in
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a, e
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Ab n
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8, re
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 In
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hi in
op fe
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, o ou
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br ise
ua as
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27 Co
-2 nfe
8, re
20 nc
10 e
Riedel et al., Nature Neurol 2006
methylprednisone 1g/day x 5 days

10 e
20 nc
8, re
Dramatic improvement in mental status

-2 nfe
27 Co
ry e
ua as
br ise
Discharged on prednisone 60mg/day

Fe D
n s
, o ou
tenofovir, lopinavir/ritonavir, zidovudine

ia cti
op fe
hi in
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a, e
ab al N
Ab n
s io
di nat
Ad ter
In
 Immune Reconstitution Inflammatory

10 e
Syndrome

20 nc
8, re
-2 nfe
27 Co
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br ise
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Fe D
n s
, o ou
clinical condition that is paradoxically
ia cti
op fe
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attributable to the recovery of the
Et uro
a, e
ab al N

immune system after initiation of ART

Ab n
s io
di nat
Ad ter
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 In
Ad ter
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Ab n
ab al N

Patients on HAART
a, e
15-25%
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op fe
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27 Co
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8, re
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10 e
EPIDEMIOLOGY of IRIS

20-45%

Shelburne et al., 2006

Patients with OI on HAART
 Time between of Initiation of HAART and IRIS

10 e
20 nc
8, re
-2 nfe
27 Co
100

ry e
ua as
Time interval (days)

br ise
75

Fe D
n s
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50

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25 hi in
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0
ab al N

0 10 20 30 40 50 60 70 80
Patients with IRIS (%)
Ab n
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Shelburne et al., AIDS, 2005 Johnson and Nath NYAS 2010

In
Treatment options for IRIS are not ideal

10 e
20 nc
Steroids:

8, re
-2 nfe
27 Co
Risks from immune suppression

ry e
ua as
br ise
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Fe D
n s
, o ou
therapy:
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op fe
hi in
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a, e
ab al N

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Ab n
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HAART/ immune restorative therapy

Ad ter
In
Recommendation for use of steroids in
IRIS

10 e
20 nc
8, re
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27 Co
steroids x 1 month (with OI prophylaxis)

ry e
ua as
br ise
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n s
, o ou
Symptomatic IRIS: high dose steroids taper with oral

ia cti
steroids (debatable) op fe
hi in
Et uro
a, e
ab al N
Ab n
s io

Asymptomatic IRIS: wait and see (debatable)

di nat
Ad ter
In
 In
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8, re
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 In
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8, re
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GBS
In
Ad ter
di nat
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Ab n
ab al N
Radiculopathy

a, e
Et uro
hi in
op fe
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, o ou
n s
Fe D
Mononeuritis multiplex

br ise
with HIV

ua as
ry e
Sensory motor neuropathy

27 Co
-2 nfe
8, re
20 nc
10 e
Peripheral Nervous System
 CMV Polyradiculitis

10 e
20 nc
8, re
-2 nfe
27 Co
Occurs late in HIV infection; CD4 usually <

ry e
ua as
100; concurrent CMV infection in >60%

br ise
Fe D
Cauda equina syndrome: asymmetric

n s
, o ou
motor, perineal sensory, back pain,

ia cti
op fe
sphincter hi in
Et uro

CSF: poly pleocytosis, n protein, p

a, e
ab al N

glucose, + CMV PCR+ in 95%

Ab n
s io
di nat
Ad ter

Rx: Induction: ganciclovir [+ foscarnet]

In

Maintenance: valganciclovir
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 In
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27 Co
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8, re
20 nc
10 e
 HIV-associated GBS

10 e
20 nc
8, re
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27 Co
Increased frequency of GBS

ry e
ua as
relative to general

br ise
population

Fe D
n s
Similar presentation to HIV

, o ou
ia cti
neg, except that CSF
op fe
hi in usually cellular
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Usually presents early in

a, e
ab al N

HIV infection
Ab n
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Presumably an immune-
di nat

mediated phenomenon
Ad ter
In

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10 e
20 nc
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27 Co
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-2 nfe
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20 nc
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Incidence of neuropathy
 Clinical features of HIV sensory

10 e
20 nc
neuropathies

8, re
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ua as
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sens. thresholds 85%
$EVHQWUHGXFHG$-V 96%
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Distal weakness 33%

Atrophy or wasting 30%
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Fasciculations 0%
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Features of HIV distal sensory polyneuropathy and

In

antiretroviral toxic neuropathy are identical. Neuropathic sx.

are correlated with plasma HIV RNA

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Skin biopsy assesses unmyelinated nerve fibers

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density and nerve fiber
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