Hypertension: There are three major things central to hypertension. They include increased systemic vascular resistance, increased vascular stiffness and increased vascular responsiveness to stimuli.

Hypertrophy: Cells increase in size to deal with increased workload. With increased vascular resistance and vascular stiffness in the circulation distal to the heart (aka increased cardiac afterload), the heart cells in the left ventricle get bigger, leading to LVH.

LVH is a relatively early response to hypertension; it is even demonstrated on echocardiogram of children and adolescents with borderline hypertension. LVH may even begin before hypertension because the same factors (angiotensin II, norepinephrine, epinephrine, increased sympathetic drive, and endothelin) promoting both HTN and LVH .

Why is LVH a problem?

•  LVH is an increased in muscle mass and wall thickness but not ventricular volume. It also leads to decreased elasticity of the heart muscle.
• It impairs diastolic function, slows relaxation and delays filling.
• It can lead to chronic pressure overload which leads to heart failure
• Complications can occur such as arrhythmia, ischemia, MI, and sudden cardiac arrest. These complications are likely due to two things. First, there is reduced density of capillaries in hypertrophied myocardium. Second, the enlarged muscle mass limits the ability of the coronary arteries to dilate and respond to decreased perfusion.
• The perfusion issues that we have just discussed can make the heart irritable and at risk of arrhythmia but there is also some remodeling of the electrical system of the heart in LVH. This could include prolongation of the action potential (i.e. leading to bundle branch block), altered repolarization and early action potentials (leading to VF, VT, torsades, or atrial fibrillation). 

• Shortness of breath
• Chest pain
• Palpitations
• Dizziness and fainting spells
• Quick exhaustion with physical activity.

• 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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Tuberculous meningitis usually presents with a non-specific clinical picture. The cranial nerves are frequently affected. Tuberculous meningitis induces an increase in the number of lymphocytes in the cerebrospinal fluid and a decrease in glycorrhachia. Acid-fast bacilli can sometimes be shown by direct examination, but in view of the low sensitivity of direct examination, a culture (Löwenstein-Jenssen) may be necessary. Nodular thickenings, i.e. tuberculomas of the meninges can be observed on CT scan or MRI.