To identify patients with GPI, cause-of-death statistics was used. In this study, MFT practice in the Dutch Vincent van Gogh psychiatric hospital in GPI patients who had been admitted in the period 1924-1954 is explored. In 1921 Wagner-Jauregg reported an impressive therapeutic success of MFT and it became the standard treatment for GPI worldwide. This year marks the 100th anniversary of the first malaria fever treatment (MFT) given to patients with general paralysis of the insane (GPI) by the Austrian psychiatrist and later Nobel laureate, Julius Wagner-Jauregg. In doing so, the hope is to raise awareness for the diagnosis of neurosyphilis, especially in the elderly patient presenting with psychiatric symptoms. The goal of this discussion is to bring awareness to this infrequent presentation and share simple examination techniques that could have been used to diagnose and treat this patient’s symptoms more promptly. This patient presented with Argyll-Robertson pupils and significant risk factors. This case study explores signs in the history and physical examination that should quickly prompt a provider to consider neurosyphilis in their differential. A routine Treponema pallidum antibody test returned positive and a further workup of confirmatory lab work, a thorough neurological exam, and magnetic resonance imaging (MRI) revealed a chronic syphilis infection. He was finally admitted with delirium, suicidal ideation, and paranoia. Due to the decreased severity of the presentation, this patient was sent home from the emergency department multiple times until the anxiety progressed to psychosis. Rarely does a 70-year-old male with neurosyphilis present simply with anxiety.
This diagnosis is often forgotten when an elderly patient is being worked up for altered mental status. The number of cases of late and late latent syphilis in the United States is on the rise. Finally, ataxia is caused by compression of the superior cerebellar peduncle.
We did not find a reasonable explanation for squint. Ptosis in Parinaud’s syndrome is caused by damage to the oculomotor nerve, mainly the levator palpebrae portion. Blurry vision is related to accommodation problems, while the visual field defects are a consequence of chronic papilledema that causes optic neuropathy. Diplopia is mainly due to involvement of the trochlear nerve (IVth cranial nerve. In Parinaud’s syndrome patients conserve a slight response to light because an additional pathway to a pupillary light response that involves attention to a conscious bright/dark stimulus. Pseudo-Argyll Robertson pupils constrict to accommodation and have a slight response to light (miosis) as opposed to Argyll Robertson pupils were there is no response to a light stimulus. External compression of the posterior commissure, and pretectal area causes pseudo-Argyll Robertson pupils.
Overstimulation of the M group of cells and increased firing rate of the CCN group causing eyelid retraction. In the vicinity of the iNC, there are two essential groups of cells, the M-group cells and central caudal nuclear (CCN) group cells, which are important for vertical gaze, and eyelid control. In Collier’s sign, the posterior commissure and the iNC are mainly involved. In CRN, there is a continuous discharge of the medial rectus muscle because of the lack of inhibition of supranuclear fibers. In upward gaze palsy, three structures are disrupted: the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF), interstitial nucleus of Cajal (iNC), and the posterior commissure. We investigated the pathophysiology related to the signs and symptoms to better understand the symptoms of Parinaud’s syndrome: diplopia, blurred vision, visual field defects, ptosis, squint, and ataxia, and Parinaud’s main signs of upward gaze paralysis, upper eyelid retraction, convergence retraction nystagmus (CRN), and pseudo-Argyll Robertson pupils. Parinaud’s syndrome involves dysfunction of the structures of the dorsal midbrain.
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