Paraneoplastic syndromes (PS) result from indirect effects of neoplasms. In 50% of the cases the symptoms precede the diagnosis and run independently. PS may involve the peripheral or central nervous system, resulting in symptoms from sensory neuropathies to several neuropsychiatric manifestations.

To review the psychiatric manifestations of paraneoplastic syndromes affecting the nervous system.

Selective literature review via PubMed search, using the keywords “paraneoplastic syndromes”, “endrocrine paraneoplastic syndromes”, “neuropsychiatric manifestations”, “limbic encephalitis”.

The prevalence of PS varies with the type of cancer (<1% for breast and ovarian cancers; 3-5% for small cell lung cancer; 20% for thymomas). The general mechanisms behind PS are related to the production of substances by the tumor that directly or indirectly cause distant symptoms, the depletion of substances or the host response to the tumor. Frequently there are autoimmune phenomena involved, with the production of antineuronal antibodies that recognise various antigens at the nervous system. Paraneoplastic neurological disorders include limbic encephalits that can present subacutely with symptoms of depression, irritability, hallucinations, cognitive impairment associated with sleep alterations, confusion and seizures. Others include psoclonus-myoclonus ataxia syndrome, neuromyotonia and cramp fasciculation syndrome. Metabolic and endocrine paraneoplastic syndromes (hypercortisolism, carcinoid tumors, pancreatic cancer) can result from the production of cytokines and hormones by the tumor and produce mood disorders, confusional states and psychosis.

PS can be related to various neuropsychiatric manifestations affecting consciousness, cognition, mood and perception. The recognition of this association can alert for the possibility of a cancer diagnosis specially when facing a patient with unusual clinical presentation.

No significant relationships.

Neurocysticercosis is a parasitic infection of the central nervous system and caused by the pork tapeworm Taenia solium. Humans become infected after consuming undercooked food or water contaminated with tapeworm eggs, or through poor hygiene practices. The clinical manifestations of neurocysticercosis (NCC) largely depend on the number, type, size, localization, and stage of development of cysticerci, as well as on the host immune response against the parasite. Seizures are the most common manifestations of NCC (70–90%) of patients, followed by headache (38%), focal deficits (16%) and signs of intracranial hypertension (ICH) (12%), but psychiatric symptoms can also be seen.

Literature review on neuropsychiatric manifestations of neurocysticercosis, based on a clinical case.

Pubmed search using the keywords neurocysticercosis, psychiatric comorbidity, neuropsychiatric manifestations.

We present a clinical case of a 29-year-old male patient, with history of an epilepsy, that immigrated to Portugal with his family from Cape Verde for specialized medical care. He presented to the ER with an acute psychotic episode characterized by disorientation, persecutory ideation, psychomotor agitation and violent behavior. Brain CT scan showed multiple calcifications in cerebral parenchyma and CSF was positive for antibodies against T. solium.

The polymorphous symptomatology seen in NCC is mimicked only by neuro-tuberculosis and neurosyphilis in developing countries, and multiple sclerosis in the Western countries. Psychiatric symptoms are a part of the clinical presentation of infectious diseases. It is important to consider NCC in endemic areas presenting with psychiatric symptoms, especially those showing poor response to the standard treatment and in those with history of seizures.

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We present the case of an 82-year-old patient who was treated by our liaison psychiatry unit after a suicide attempt through prescription-drug overdose. The patient had been diagnosed with Parkinson’s disease (PD) ten years prior to his admittance and was being treated with carbidopa/levodopa and non-ergot dopamine agonists.

Impulse control disorders and depression are the most prevalent neuropsychiatric manifestation of PD. According to several sources, this symptomatology is underdiagnosed and undertreated, causing helplessness and distress to patients and their caregivers. Likewise, the accumulated evidence suggests that certain drugs can contribute to the appearance of the aforementioned symptoms.

A case report is presented alongside a review of the relevant literature regarding the neuropsychiatric manifestations in the context of PD and the diagnosis and treatment of these symptoms.

During his treatment, ropinirole was removed while quetiapine was progressively administered (up to 150mg/day). Carbidopa/levodopa regime was increased causing visual hallucinations and delusional jealousy. A careful balance between antiparkinsonian and antipsychotic medication needed to be achieved before discharge.

Neuropsychiatric manifestations in the context of PD are more prevalent than what was thought in the past. Certain medications, particularly non-ergot dopamine agonists could potentially contribute to the onset of these symptoms. Moreover, these manifestations can be underdiagnosed due to the stigma or social burden imposed upon family and / or caregivers. It is important that recent advances in the understanding of non-motor symptomatology of PD could permeate clinical practice to achieve an adequate identification and treatment of these symptoms.