Brain abscess & trigeminal neuralgia

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Information about Brain abscess & trigeminal neuralgia
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Published on March 12, 2014

Author: magician10k

Source: slideshare.net

Etiology  Organism: Streptococcus; Klebsiella , Staphylococcus aureus, and anaerobes.  In immunocompromised patients, it is important to include Toxoplasma, and Nocardia as possible etiologic agents, as well as fungal pathogens.  Source: Classically, these abscesses arise locally from otorhinolaryngeal infections like (Sinus, ear, dental infections ) Or Hematogenously from distant infections. Or Head trauma( blunt, penetrating ,surgical)

Clinical picture  Headache, nausea, vomiting, and altered mental status can occur due to increased intracranial pressure, while unilateral headache, seizures, and many focal neurological deficits occur due to the presence of a mass lesion. Fever and nuchal rigidity are also seen in many cases.  Investigation The key to diagnosing brain abscess is correlating the clinical scenario with an imaging study, such as contrast-enhanced CT or MRI. The classic finding on CT or MRI is a circular lesion with a strongly contrast-enhancing surround rim.

Treatment  Treatment should also be aimed at correcting the primary source of infection .  Initial surgical treatment usually consists of needle aspiration of the abscess. A total excision can be performed if the abscess is chronic, and encapsulated .  Antibiotic therapy typically consists of 6 to 8 weeks of intravenous treatment followed by 4 to 8 weeks of oral treatment.  Patients should receive routine follow-up imaging and should also be started on an antiepileptic medication.  Glucocorticoids should be considered to counteract symptomatic intracranial hypertension, although their role is less important than in the treatment of brain tumors.

Anatomy

Introduction  Neuralgia  Unexplained peripheral nerve pain  The most common site: head and neck  The most frequently diagnosed form: trigeminal neuralgia (TN)  Female predominance (male : female = 1:2)

Characteristics of trigeminal neuralgia  paroxysms of severe, lancinating , electric shock-like bouts of pain restricted to the distribution of the trigeminal nerve  Unilaterally  The mandibular and/or maxillary branch or, rarely, the ophthalmic branch

 Spontaneous attacks or triggered by trigger zone & movement of the face  Seconds to minutes.  During an attack of TN, the sufferer will almost always remain still and afraid from speech or movement of the face, so as not to trigger further attacks of pain.

Pathogenesis of trigeminal neuralgia  Traumatic compression of the trigeminal nerve by neoplastic (cerebellopontine angle tumor) or vascular anomalies  Infectious agents  Human herpes simplex virus (HSV)  Demyelinating conditions  Multiple sclerosis (MS)

Treatment  Medical treatment  Carbamazepine (Tegretol) – first line  Oxcarbaazepine  Gabapentin (Neurontin)  Lamotrigine  Baclofen  Phenytoin  Clonazepam  Valproate  Mexiletine  Topiramate Second line Others

 Surgical treatment  Gasserian ganglion-level procedures  Microvascular decompression (MVD)  Ablative treatments  Radiofrequency thermocoagulation (RFT)  Balloon compression (BC)  Stereotactic radiosurgery (SRS)  Peripheral procedures  Peripheral neurectomy  Cryotherapy (cryonanlgesia)  Alcohol block

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