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• Acute aseptic HIV-meningitis, chronic HIV-meningitis, HIV encephalopathy (AIDS dementia), vacuolar myelopathy, predominantly sensory neuropathy, inflammatory demyelinising polyneuropathy, mononeuritis multiplex, myopathy.
  
• Cerebral toxoplasmosis, Cryptococcus meningitis, tuberculous meningitis, CMV retinitis-encephalitis-radiculitis, herpes encephalitis, progressive multifocal leukoencephalopathy (JC virus), neurosyphilis, primary cerebral lymphoma, metastatic systemic lymphoma.
  

• Toxoplasmosis: by far the most frequent
  
• Primary CNS lymphoma
  
• Mycobacterium tuberculosis
  
• Mycobacterium avium complex
  
• Progressive multifocal leukoencephalopathy
  
• Cryptococcus neoformans
  
• Candida sp.
  
• Listeria monocytogenes
  
• Nocardia asteroides
  
• Salmonella group B
  
• Aspergillus sp.
  
• Rhodococcus sp.
  
• Acanthamoeba sp.
  
• Syphilitic gumma (syphilis, Treponema pallidum)
  
• “Classical” bacterial cerebral abscess, e.g. otogenic, from sinus, secondarily to endocarditis.
  

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• Temporal lobe abscess: ipsilateral headache, aphasia, upper homonymic quadrant anopsia.
  
• Frontal lobe abscess: headache, dizziness, confusion, diminished mental capacity, hemiparesis, motoric speech disorders.
  
• Parietal lobe abscess: headache, visual disturbances.
  
• Cerebellar abscess: nystagmus, ataxia, dysmetria, vomiting.
  

• Ring-enhanced single lesion: abscess, with frequency toxoplasmosis > TB > cryptococcosis. The peripheral staining by the contrast medium shows the oedema zone around the abscess. On this basis a test therapy will often be started without having formal proof of toxoplasmosis. If there is no improvement within two weeks or if deterioration occurs, a stereotactic brain biopsy should be performed. In addition to these three etiologies, there can be other causes of an intracranial mass: herpes, Histoplasma, Nocardia, Candida, Kaposi, metastasis. In 10% of cases no specific cause is found.
  
• Non-ring enhanced lesion: probably lymphoma > PML. In case of PML there is no mass effect.
  
• Bilateral diffuse lesions: immune reconstitution syndrome if in the correct context.
  
• Multiple ring lesions: toxoplasmosis >> tuberculosis.
  
• HIV atrophy: broadened sulci and enlarged ventricles (DD internal hydrocephalus: flattened sulci and enlarged ventricles).
  

• Direct investigation: amoebae, trypanosomes, filaria
  
• Cell counts: type and number (nl < 3/mm³)
  
• Biochemistry: protein content (nl 25-40 mg%), glycorrhachia (nl 40-90 mg%, nl 50-80% of the glycaemia)
  
• Serology: Syphilis, intrathecal production of various antibodies (compare with titre in serum sample)
  
• Antigen-detection: Cryptococcus
  
• PCR: Mycobacteria, JC virus, herpes, toxoplasmosis
  
• Stains: Gram, Indian ink, Ziehl
  
• Culture: virus, bacteria, mycobacteria, fungi
  
• Cytology: only in case of suspected carcinomatous meningitis
  

Dark brown (on black skin) or purplish plaques and nodules (on white skin) on the skin or reddish-purple elevations in the mouth indicate Kaposi's sarcoma. This is a cancer that can affect any part of the body (lung, intestine, eye etc.) in AIDS patients, in contrast to the so called endemic Kaposi in Africa, which develops slowly and usually causes lesions only on the feet and legs. [Note: The disease was first described in 1872 by Moritz Kaposi, a Hungarian dermatologist. The disease is encountered principally in persons from Eastern Europe and the Mediterranean basin]. Kaposi's sarcoma thus occurs less frequently in Southeast Asia than in Africa. Since Kaposi's sarcoma occurs much more frequently in homosexual men than in patients infected with HIV via blood, an infectious cause was suspected. Kaposi's sarcoma also occurs more frequently in HIV-negative transplant patients. Immunosuppression appears to be needed for expression of the agent. A new herpes virus genome (KSHV [Kaposi's Sarcoma Herpes-like Virus] or HHV-8 [human herpes virus 8]) was found in the DNA of Kaposi's sarcoma cells and certain lymphomas. This virus apparently has a causal role in these cancers (and also in a variant of Castleman’s disease, a lymphoproliferative disease of B-cells). The virus is found in sperm, though much higher concentrations occur in saliva. This virus is also suspected of playing a role in pulmonary hypertension, but more research is needed.

• α-herpes virus, e.g. Herpes simplex virus 1 and 2, Varicella zoster virus (= HHV3)
  
• β-herpes virus, e.g. Cytomegalovirus (HHV5), Roseolovirus (= HHV6) and HHV7
  
• γ1-herpes virus, e.g. Epstein-Barr virus (= HHV4)
  
• γ2-herpes virus, e.g. Kaposi's Sarcoma Herpes Virus (HHV8)
  

Anterior segment

Posterior segment

• Apomorphine (and Bromocriptide)
• A D₂ agonist used in the treatment of parkinsons
• It acts on the D₂ receptor in the CTZ to cause vomiting
• Morphine
• In excess amounts, also acts on D₂ receptors
• Syrup of Ibericat
• Irritates the gut, causing activation of 5HT₃ receptors
• Cisplatin
• Anti cancer drug which causes release of serotonin in the gut, which then acts on 5HT₃ receptors

• The main area in the brain responsible for vomiting is the vomiting center
• This area is located in the lateral reticular formation of the medulla
• It receives input from many areas:
• Chemoreceptor trigger zone
• Located in the floor of the 4th ventricle in the area postrema
• It picks up circulating chemical in the blood
• It is important because it lies outside the BBB, therefore, circulating toxins (e.g.bacterial food poisoning toxins, chemotherapy) can cause vomiting, even though they do not pass through the BBB

• Vestibular apparatus
• Tractus solitarius
• vagal afferents from the gut, heart and testes
• Direct input from gut (reflex)

• On the CTZ:
• 5HT3
• D2
• On the vagal afferents:
• 5HT3
• In the vomiting center
• Muscarinic
• H1 receptors

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