Diseases information. Disorders. Treatment.

Syphilis. Secondary stage is when you get meningovascular syphilis. If you have a 35-year-old person with a stroke, think meningovascular syphilis. In the secondary stage you can have a meningitis. It’s a subacute meningitis, catches cranial nerves very easily, just like TB. Second, third, sixth, all kinds of cranial nerves are caught. Subacute meningitis in a young person, the tempo is a little slow, keep syphilis in mind. The tertiary stage which comes five, six years after the primary exposure, the secondary stage comes about two or three years after exposure. That’s when you get meningitis and stroke. The tertiary stage comes after five or ten years. There are two disorders you need to remember. One, obviously is tabes dorsalis; shooting pain, proprioceptive loss, ataxia, bladder problem with Argyll-Robinson pupil. Tabes dorsalis. Charcot’s joints. Big destroyed swollen joints. Tabes dorsalis. GPI is general paralysis of the insane. Subacute or short chronic dementia. Personality change, dementia coming on over 4-6 months in a 45-year-old person. Rather than a 70-year-old person with two year dementia, which is Alzheimer’s. GPI is four, five, six months of dementia. Very important. They have motor findings; dysarthria, hip tremor, provigil. GPI.

Cysticercosis. The fluid that the cyst has apparently is very irritating to the brain. In fact, people apparently die when you remove the cyst. So treat with praziquantel or albendazole. Occasionally you may need to shunt. If the patient just has seizures, give them seizure drugs.
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Slow viruses. Kuru, New Guinea, Creutzfeldt-Jakob, dementia, myoclonus, basal ganglia problems. Maybe cortical blindness, maybe ataxia, periodic complexes. The CSF is normal. They die in about a year, at the most two. PML we talked about. JC virus, white matter. What does this do? Gertsmann’s-Strausler syndrome? What’s the main sign and symptom? Cerebellar ataxia, positive family history. So the differential diagnosis for Creutzfeldt-Jakob in a way is Gertsmann’s-Strausler. But look carefully for family history. SSPE: post-measles, younger people. The EEG complexes are high in amplitude but less frequent.

HIV. If your CD4 count is reasonable, an HIV patient is more likely to have stroke. He can have a meningitis. Now as the CD4 drops you go through TB and then AIDS-related dementia. Now when the count is very low you get PML, CMV lymphoma zoster. And crypto comes under here. So this is going to be of some practical use in differential diagnosis when you are dealing with these guys. There is no absolute rule here. CD4 is the lymphocytes that the AIDS virus affect, that destroy them. The clue for toxoplasmosis, very early focal signs. MRI lesions light up. Almost always basal ganglia is involved on MRI. Here is the treatment. Pyrithiamine sulfa. Clindamycin can be useful. Now you need to prevent toxo with half dose of these drugs. So once you treat them for four, six, eight weeks, keep the patient on maintenance dose because the toxo does recur. The maintenance dose is usually half the therapeutic dose. Canadian pharmacy
Lymphoma: subacute onset. The lesions cross the midline then you find lesions close to the ventricles. The focal findings will be very similar to toxo sometimes but if MRI lesions cross the midline, think lymphoma. One you get toxo once, you are going to get it again. They need maintenance. Maintenance means maintenance for the rest of their life. You can look for Epstein-Barre PCR in the biopsy specimen, if the lesion is lymphoma. It’s not very sensitive but you may pick the virus particles in about 30 or 40% of lymphomas. If you are not sure between toxo and lymphoma, obviously you need to go for biopsy. Crypto: clues, retinitis. If the scenario is a patient with AIDS, low CD4 count, has some visual blurring and has headache, think crypto. Polyradiculitis is common. It can catch the cranial nerves. PML: you saw PML JC virus. Symmetric demyelination on MRI. PML lesions do not enhance. That’s important. PML lesions do not enhance. Toxo enhances, lymphoma enhances. Lymphoma crosses the midline. Zoster, myelitis is common. CMV can produce myelitis. CMV can produce myeloradiculitis. CMV can produce polyneuropathy. There are a whole bunch of differential diagnoses. Any one of them can produce myelopathy. So if an AIDS person comes to you with transverse paraplegia on a sensory level it can be pretty tricky. A lot of times you may end up doing a bone marrow biopsy looking for toxo, look for PCR. The whole works. Sometimes you never find out.
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HIV dementia complex. In children dementia is more common than infections, whereas in adults, infections are more common than dementia. Big, funny, giant cells. Atherogenesis is still a little bit uncertain. They don’t know how the virus actually affects the neurons. There are all kinds of theories here. Treatment for dementia: there is some evidence that treatment works for dementia. HIV myelopathy is the so-called vacuolar myelopathy slowly ascending. Numbness in the feet, legs stiff, legs weak. A month later the arms go numb and weak. So ascending myelopathy. Whereas infective myelopathy is more acute, definite transverse level. You can have myopathy very similar to polymyositis. AZT can produce myopathy. During seroconversion you can have a transient aseptic meningitis-like picture. Headache, throwing up for a week, then you get better. The virus can produce a chronic aseptic meningitis as well. So if you have a chronic meningitis on top of all the fungal stuff, you need to think of direct HIV meningitis also.

Now all these drugs can apparently produce headache and a bunch of cells in CSF. Never seen one, but the books mention those. Methotrexate of course we know. Apparently this is an immunosuppressant drug. We talked about CSF glucose, we talked about lactate being normal, tumor necrosis factor being low. In bacterial, these two are high.
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Low sugar is very important. Keep that in mind. Now TB meningitis, cancer of the meninges and Toxoplasmosis a lot of times produce a lot of protein in the CSF. Like you are looking at 500, 600 mg. TB meningitis is notorious. You get like 1.2 grams of protein. So if you have a very high protein, think those first: TB, cancer and Toxoplasmosis. You can look for fungal antigens, viral antigens, but those things take time so they are not going to help you on the same day. I forgot to mention Lyme’s, polyradiculitis, and meningoencephalitis, look for Lyme antibody. I’m going to talk about HIV at the end of the talk.

Herpes simplex and TB. If you suspect Herpes simplex encephalitis, your differential is viral meningitis, obviously look at EEG. Start them on acyclovir but you can do PCR for herpes virus.
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Fungal meningitis. Regional distribution is important. In the Southwest coccidioides is a common cause. If you have patients on hemodialysis, IV drug use, hyperalimentation, go for Candida first. In the Mississippi valley, with an abnormal chest x-ray, obviously go for TB and also go for histo. We have seen histo in our place from time to time. Treatment: amphotericin B. Remember fever, rash, kidney toxicity, anemia, low platelet, low potassium. Flucytosine: bone marrow, GI, confusion, liver, rash, stones. Fluconazole: especially for HIV crypto-maintenance - I’m going to talk about it - this is a new antifungal drug. I can’t tell you anything more about it than how to spell it. Probably when others don’t work. This is a fairly new drug. But still the standard drug is amphotericin B and flucytosine.
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In viral encephalitis, patients are more sick, altered mental status, focal findings, abnormal EEG. Herpes simplex of course. Eastern Equine: high morbidity. Western Equine encephalitis is more benign. Low morbidity. Outside the United States, Japanese and Venezuelan encephalitis is pretty common. Now all these are seasonal, mosquito-borne. Uncommon causes of encephalitis: Rocky Mountain Spotted disease, Lyme, Leptospirosis - this is very rare, very high mortality. Two types of ameba. Non-seasonal, endemic, Herpes simplex: If you are immunosuppressed, remember Zoster varicella. Immunosuppressed, Herpes simplex 6: these are not uncommon, toxo immunosuppressed. Work-up, there is nothing magical here. Acyclovir, we know about it. If you have CMV ganciclovir. If you are dealing with Rocky Mounted Spotted Fever go for tetracycline, chloramphenicol group of drugs.

If you have meningitis with trauma, post-op or shunt situation, make sure you are giving vancomycin. Now steroids in childhood meningitis is still a little bit controversial but I think most people now recommend a few days of steroids, especially children with meningitis. Especially if you happen to have H. influenza. Two, three or four days. Some people recommend two days of Decadron. This is basically to reduce the morbidity, brain edema, ICT due to tumor necrosis factor. So there is a lot of inflammation that can trigger brain edema. So steroids are supposed to reduce that.
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What about contacts for Neisseria meningitidis? Rifampin for a few days. Family members, school contacts. Rifampin is the way to go. For H. influenza Rifampin is for the contacts also. Here’s a list for strep, Neisseria, H. influenza, Listeria. Ampicillin. If you have a gram-negative situation a whole lot of different combinations there, including metronidazole. Proteus, Pseudomonas, gentamycin. Staph aureus, vancomycin. So this again is pretty easy. This may vary from this list to your people. Nothing is carved in stone. Talk to your ID people. There may be some subtle variations on the theme. TB meningitis is associated with a very high risk of stroke, compression of optic nerve, extremely high protein, big time risk of hydrocephalus, basal adhesions. So steroids in TBM is accepted by most people.
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Viral meningitis. Patients are less sick, no focal features. CSF shows lymphocytes, glucose is normal. Easy. Here is a list of some of the common causes you look for. Enteroviruses, echo, Coxsackie B, polio, mumps, Herpes simplex I and II, Varicella zoster, Epstein-Barre, adenovirus, lymphocytic choriomeningitis, occasionally Influenza A and B. Now the differential diagnosis of viral meningitis includes partly treated bacterial meningitis. Look for cultures, look for how sick the patient is, look for antigens. Continue, in many cases, as if the patient has bacterial meningitis if you are not sure. One of the very important diagnostic helps in partly treated bacterial meningitis is EEG. EEG in viral meningitis is essentially normal but in bacterial meningitis, even if partly treated, often shows slow waves. So the EEG can be a very helpful test when you want to differentiate the two phenomena. Fungal meningitis produces a lot of lymphocytes. What’s the one important CSF change, the difference between virus and fungus? Glucose. In fungus, the glucose is low. In TB meningitis glucose is low.

What about spinal abscess? Pretty uncommon, but differential diagnosis is humongous. Acute pain, paraplegia, you have to think all kinds of things. Especially the neurosurgeons in the audience. Before we get the MRI the problem may be metastases, the problem may be blood, spinal AVM. Maybe anticoagulants, obviously disc. Think of medical problems; stroke in older people. You can have pain with stroke, spinal cord stroke. Dissection, hypertension are important factors that produce spinal infarction. Lupus myelopathy, cocaine can produce vasculitis, sarcoidosis can produce acute myelopathy with pain. This is post-infection myelitis, so look for preceding infection. So the differential diagnosis of acute spinal cord syndrome is pretty big.
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Shunt infection. Incidence, approximately 10% or less, higher after the first shunt. Higher in children, small children. Higher if the surgeon is less experienced. This is what the literature says. So these are the risk factors for shunt infection. They usually come within a few weeks of the first shunt insertion. Look for cells, fever, meningeal signs.
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Bacterial meningitis. Strep, pneumonia, one out of four strep meningitis is now penicillin resistant. H. influenza B we don’t see anymore because of vaccination. Listeria is getting more common, especially in older people with meningitis. Strep pneumonia still carries very high morbidity and mortality. Neonates, strep pneumonia is now a number one cost. Listeria is becoming more common in the neonate. Morbidity seems to relate to cerebral edema and intracranial pressure. If you have venous thrombosis and stroke, you have higher morbidity. Many people with bacterial meningitis have vasculitis of the skull base. They get stroke. You can have subdural empyema after meningitis, you can have abscess with meningitis. So if you start out with meningitis, you treat the patient for two or three days, the patient then develops focal findings. The differential diagnosis would be stroke, venous thrombosis, abscess forming or empyema forming. So those are the three or four complications you need to remember. This keeps coming up. If the patient is not deeply comatose, if there are no focal findings, if there is no papilledema. It’s okay to take little bit of CSF out if you suspect meningitis. Then it’s also okay to start antibiotics. One or two doses is not going to change your CSF very much. Of course typical findings in CSF is a lot of polymers, high sugar, low glucose. We all know that. You can look for bacterial antigens in just about all those situations by latex testing. Lactate in the CSF can be helpful. Lactate goes up if you are dealing with bacterial meningitis. Lactate is not increased in viral meningitis. Tumor necrosis factor is still experimental. It is increased in many people with bacterial meningitis.

Supratentorial neurosurgical infections. One is abscess, the second is epidural empyema, and subdural empyema, which statistically is not as common. Whenever you have infection in the supratentorial compartment hitting one side of the brain, always remember Herpes simplex encephalitis as the differential diagnosis. Because the symptoms and signs can be pretty similar. What are they? Focal cerebral signs, hemiplegia, focal seizures, field defects, aphasia, plus fever. Now the weakness, if you have a stroke, tends to be very severe and more abrupt. But if you are dealing with infections, the tempo is a little bit slow, the weakness is not like stroke. Grade IV, maybe grade III, mild or moderate. Knee problems

Brain abscess. Look for local source of infection; ear, tooth, maybe skin, maybe trauma, maybe systemic. May be endocarditis, maybe IV drug use. If you look at the abscess pathologically or with MRI the pinnar surface is close to the ventricle. You need to remember that. So it kind of ruptures easily into the ventricle. Remember the wall is thinner on the ventricular side. What are the bugs? A whole bunch of them. Very often it’s more than one. Now for exam purposes let me just point out a couple here. If you have local trauma, staphylococcus is the common offending bacteria. In the neonate all these can cause brain abscess. Treatment; if the abscess is small, many books talk about less than 3 cm diameter, antibiotics for 2-3 months is probably enough. If the abscess is big - obviously even those small abscesses you need to follow with MRI or at least CT. Here’s the list of antibiotics for you. Now if the abscess is big, antibiotics and aspiration. So pretty straightforward kind of stuff. The factors that affect the prognosis; size, larger the abscess the worse the outcome, and then when you get them. If the patient is already comatose before treatment is started, prognosis is worse. Of course if their abscess has already ruptured, pretty difficult. If you have ventriculitis, a lot of those people just don’t make it.
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If you have pus collection in the meninges, epidural or subdural, these people on the whole tend to be a little younger and seizures are more common. Seizures, in fact in my experience, are almost universal - if you are dealing with empyema - because they get a lot of cortico-thrombophlebitis so you have more irritation of the gray matter, so seizures are more common. Meningeal signs are more common in epidural as well as subdural. The treatment principles are the same. Remove the pus, antibiotics, watch with MRI.