What causes slurring of speech, dysphagia (difficulty swallowing), and involuntary head movement in Human Immunodeficiency Virus (HIV) patients?

Neurological Symptoms in HIV: Causes of Slurred Speech, Dysphagia, and Involuntary Head Movements

The combination of slurred speech, difficulty swallowing, and involuntary head movements in HIV patients most commonly results from HIV-associated dementia (HAD), opportunistic infections affecting the basal ganglia and brainstem (particularly toxoplasmosis), or less commonly, medication-related movement disorders. 1, 2

Primary Diagnostic Considerations

HIV-Associated Dementia (HAD)

HIV-associated dementia presents with a characteristic clinical triad: cognitive dysfunction, motor abnormalities (including dysarthria and dysphagia), and frontal release signs, representing a subcortical dementia syndrome. 1

• This occurs most commonly in patients with severe immunosuppression (CD4+ count <200/mm³) and represents direct HIV-mediated neurotoxicity through persistent immune activation and virus-induced damage 1
• Motor abnormalities in HAD can manifest as slurred speech, difficulty swallowing, and movement disorders due to subcortical involvement 3, 4
• Neuroimaging typically shows global cerebral atrophy with ill-defined T2 hyperintensities in white matter, distinct from focal lesions 1

Opportunistic Infections: Toxoplasmosis

Toxoplasmosis of the basal ganglia is the leading cause of involuntary movements in HIV patients, particularly hemichorea/hemiballismus, and can affect speech and swallowing when involving critical motor structures. 2

• In one case series, all patients with hemichorea/hemiballismus had toxoplasmosis of the basal ganglia, predominantly affecting the right side 2
• Toxoplasmosis can also cause secondary parkinsonism and hemidystonia when affecting the midbrain and basal ganglia 2
• These focal lesions appear distinct on imaging from the diffuse changes of HAD 1

Other Opportunistic Infections

Additional CNS opportunistic infections must be considered in severely immunocompromised patients, particularly those with CD4+ counts <200/mm³. 3, 4

• Cryptococcal meningitis, CMV encephalitis, and tuberculosis can all cause neurological symptoms including motor dysfunction 3, 5
• Progressive multifocal leukoencephalopathy (PML) caused by JC virus reactivation can present with motor deficits, though typically causes demyelination rather than movement disorders 6

Active HIV-Associated Brain Injury (HABI)

CSF HIV RNA escape represents compartmentalized HIV replication in the CNS and can cause rapidly progressive neurological disease with motor symptoms. 3, 6

• This occurs due to inadequate antiretroviral therapy (ART) penetration into the CNS, resistance, or poor adherence 3, 6
• Can present with diffuse white matter signal abnormality on MRI and progressive neurological symptoms 3
• CD8 encephalitis, a severe inflammatory disorder with T cell infiltration causing brain swelling, can occur in patients on ART and presents with progressive neurological deficits 3

Immune Reconstitution Inflammatory Syndrome (IRIS)

IRIS can occur within weeks to months after ART initiation and may cause severe neurological symptoms including motor dysfunction. 3, 6

• Results from immune response directed at HIV viral reservoirs in the brain 3
• Can lead to potentially fatal T cell encephalitis with brain edema 3
• Responsive to corticosteroids in severe cases 3, 6

Medication-Related Movement Disorders

Antiretroviral medications and other drugs used in HIV treatment can cause secondary movement disorders. 2

• Metoclopramide-related parkinsonism has been documented in HIV patients 2
• Efavirenz has the greatest frequency of neurologic side effects among newer ART regimens 7

Critical Diagnostic Algorithm

When evaluating these symptoms in HIV patients, immediately assess:

1. Immune status: CD4+ count <200/mm³ indicates high risk for opportunistic infections 1, 4
2. ART status: Determine if patient is on treatment, adherent, and virologically suppressed 3, 6
3. Timing: Acute onset suggests opportunistic infection; subacute suggests HAD or IRIS 3
4. Neuroimaging: MRI to distinguish focal lesions (toxoplasmosis, lymphoma) from diffuse changes (HAD, PML) 1, 6
5. CSF analysis: Check for HIV RNA, opportunistic pathogens, and inflammatory markers 3

Management Priorities

The cornerstone of management is optimizing antiretroviral therapy with agents that have good CNS penetration to suppress CSF viral replication. 1

• Never interrupt ART in patients with suspected CNS complications, as continued viral suppression is essential for immune recovery 6
• Treat identified opportunistic infections aggressively (e.g., pyrimethamine and sulfadiazine for toxoplasmosis) 3, 4
• Consider corticosteroids for severe CD8 encephalitis or IRIS with brain edema 3, 6

Critical Pitfalls to Avoid

• Do not assume all neurological symptoms are due to a single cause—multiple etiologies can coexist in HIV patients 6, 2
• Do not delay lumbar puncture in immunocompromised patients with normal CSF cell counts, as they may still have CNS infections 3
• Do not miss CSF HIV RNA escape in patients with progressive disease despite plasma viral suppression 6
• Do not stop ART when CNS complications are diagnosed; this worsens outcomes 6