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Pal Basmaga

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This page summarizes key neurological conditions, their characteristics, and differentiating factors from the CBL.

Key Neurological Conditions

Clinical Presentation: Worsening generalized headache, increasing obtundation, neck stiffness, fever (38.7°C).
CSF Findings: Cloudy CSF, low glucose (32 mg/dl), high protein (146 mg/dl), high WBC count (3800, 95% PMNs), presence of RBCs.
Complication: Hydrocephalus (due to scarring obstructing CSF flow or reducing reabsorption).

Clinical Presentation: Sudden severe headache, loss of consciousness, afebrile.
Imaging: Extensive subarachnoid hemorrhage at the base of the brain on CT scan.
CSF Findings: Many red blood cells, no white blood cells, slightly increased protein, normal glucose.
Pathology: Weakness in cerebral arterial wall (often Circle of Willis), rupture causes bleeding into subarachnoid space.

Clinical Presentation: Worsening headache, increasing obtundation, cough and fever history.
Imaging: Solitary mass lesion with ring enhancement on CT scan (e.g., in parietal lobe).
Biopsy: Granulation tissue with adjacent collagenization, gliosis, and edema.
Pathology: Healing inflammatory response, collagen deposition around the lesion, increased vascularity and disrupted blood-brain barrier cause ring enhancement. Common source: lung infection.

Clinical Presentation: Headaches, difficulty concentrating, odd behavior, generalized tonic-clonic seizure.
Imaging: Large mass with extensive necrosis, often extending across corpus callosum (butterfly glioma).
Pathology: Highest-grade glioma, most malignant primary brain tumor, rapid and extensive growth. Usually supratentorial in adults.

Clinical Presentation: Sudden loss of consciousness, high blood pressure (e.g., 160/95 mmHg).
Imaging: Area of bright attenuation (acute blood) on CT scan (e.g., in basal ganglia), effacement of lateral ventricles, midline shift.
Mechanism of Death: Cerebellar tonsillar herniation due to mass effect.

Clinical Presentation: Tinnitus, progressive unilateral hearing loss. Other cranial nerves intact.
Physical Exam: Marked decrease in hearing on one side, Rinne test: air conduction better than bone conduction.
Imaging: Solitary, circumscribed mass in the cerebellopontine angle.
Prognosis: Usually benign, resection without recurrence is likely (though hearing loss is a consequence).

Clinical Presentation: History of transient ischemic attacks (TIA), sudden onset of hemiparesis.
Imaging: Cystic area (old infarct) on MR imaging (e.g., in frontal-parietal region).
Etiology: Most result from thromboembolism, often from the heart (e.g., mural thrombus from myocardial infarction due to coronary atherosclerosis).

Clinical Presentation: Changes in sensation in legs, distal, symmetric, primarily sensory polyneuropathy, non-healing ulceration (diabetic foot). History of myocardial infarction.
Lab Findings: Elevated serum glucose (e.g., 195 mg/dl).
Pathology: Common form of peripheral neuropathy, often associated with severe peripheral vascular atherosclerosis.

Clinical Presentation: Seizure disorder, history of emigration from endemic area (e.g., Mexico City). Afebrile.
Imaging: Rounded cysts in brain cortex and/or subarachnoid space, non-enhancing.
CSF Findings: Colorless CSF, normal pressure, normal protein and glucose, few WBCs (monos/PMN).
Etiology: Infection by Taenia solium (pork tapeworm) larvae. Cysts can obstruct CSF flow leading to hydrocephalus.

Clinical Presentation: Headaches, chronic cough (smoking history). No localizing neurologic signs.
Imaging: Solitary lesion at grey-white junction, often no ring enhancement (can vary).
Etiology: Common primary sources include lung and renal carcinomas (especially in men with smoking history).

Clinical Presentation: Rapidly ascending paralysis (feet to legs, trunk, arms), variable sensory changes, afebrile, mentally alert, can become ventilator dependent.
CSF Findings: High protein (86 mg/dl), normal glucose, very few cells (e.g., 3 mononuclear cells/microliter). This is known as albuminocytologic dissociation.
Preceding Event: Most cases are preceded by a viral infection (e.g., Campylobacter jejuni enteritis) due to an immunologic mechanism (molecular mimicry).
Treatment: Plasma exchange and intravenous immune globulin (IVIG).

Bacterial Meningitis vs. Subarachnoid Hemorrhage:

Meningitis: Fever, cloudy CSF, very high WBC (PMNs), low CSF glucose.
SAH: Afebrile, sudden severe headache, clear CSF with many RBCs but no WBCs, normal CSF glucose.

Bacterial Abscess vs. Glioblastoma vs. Metastasis:

Abscess: History of infection (e.g., lung), ring enhancement, biopsy shows granulation tissue/fibrosis.
Glioblastoma: Rapid onset of symptoms, large mass with extensive necrosis, often crosses midline.
Metastasis: History of primary cancer (e.g., lung), often solitary lesion at grey-white junction, can be non-enhancing.

Guillain-Barré Syndrome vs. Other Neuropathies:

GBS: Rapidly ascending paralysis, albuminocytologic dissociation in CSF (high protein, low cells), often preceded by infection. Absent or depressed deep tendon reflexes.
Diabetic Neuropathy: Distal, symmetric, sensory polyneuropathy, non-healing ulcers, elevated blood glucose.

Cysticercosis vs. Other Brain Lesions:

Cysticercosis: History from endemic area, non-enhancing cysts (often multiple) in cortex/subarachnoid space.
Other lesions (abscess, tumor) often show enhancement.