Acute Cognitive Decline / Acute Psychosis


Also, this paper discusses in detail about the following
  • Always rule out secondary causes of psychosis before making a diagnosis of primary psychosis 
  • Treatable causes should always be considered
  • Complete work up in acute set up should be done especially if outpatient work up cannot be guaranteed. 
Differential Diagnosis of excitable malignant catatoniaCase 40-2013  
  • Infection
    • Meningitis, encephalitis
    • Other infection: In a young, healthy patient, it is unlikely that pneumonia or pyelonephritis would be manifested by altered mental status, but pulmonary aspiration caused by a toxic ingestion and vomiting would be a concern 
  • Toxic Encephalopathy
    • It takes hours or days for the results of toxicologic studies to become available, and thus emergency department clinicians must determine the initial treatment on the basis of the early clinical signs and symptoms that were observed after a toxic substance was taken 
      • Sympathomimetic Agents 
        • Amphetamines or Cocaine commonly present with tachycardia, hypertension, anxiety, psychomotor agitation, diaphoresis, and mydriasis, and such patients may have psychotic, self-destructive behavior. Seizures can occur. 
      • Sedative or Ethanol Withdrawal 
        • Similar to sympathamimetic agents including seizures; patient on BZD, seizures can present with status epilepticus 
        • Tremors may be more prominent 
        • Visual hallucinations are the hallmark of severe ethanol withdrawal (DT)
      • Anticholinergic Agents (atropine and its congeners and cyclic antidepressants)
        • altered mental status, tachycardia, mydriasis, acute urinary retention, decreased bowel sounds, and fever are common, 
        • but do not cause diaphoresis 
        • “dry as a bone, blind as a bat, red as a beet, hot as an oven, and mad as a hatter.” 
      • The Serotonin Syndrome and the Neuroleptic Malignant Syndrome
        • Serotonin syndromeagitated delirium, autonomic dysfunction (fever, tachycardia, hypertension, and diaphoresis), and neuromuscular hyperactivity. 
        • The neuroleptic malignant syndrome is characterized by fever, muscular rigidity, altered mental status, and autonomic instability in patients who recently have begun taking a prescribed neuroleptic medication or have had a dosage increase 
        • Drugs obtained on the street frequently contain unexpected substances, and so these diagnoses cannot be dismissed even when patient is not taking serotonergic or neuroleptic substances 
      • Anion-Gap Acidosis
        • two toxic substances cyanide and toxic alcohol (methanol or ethylene glycol) have effective antidotes. 
        • sodium thiosulfate reacts with cyanide to form the nontoxic thiocyanate, and 
        • fomepizole (4-methylpyrazole), an alcohol dehydrogenase inhibitor limits the toxic effects of methanol and ethylene glycol 
      • Bath Salt intake
        • Synthetic derivatives of cathinone, a sympathomimetic chemical found in the leaves of the khat plant (Catha edulis
        • Cathinones are closely related to other sympathomimetic amines, such as amphetamines and ephedrine, differing only at the β-carbon of the propyl side chain. At the β-carbon position, an absence of substitution is representative of amphetamines, the presence of a ketone group (known as β-keto) is characteristic of a cathinone, and the presence of a hydroxyl group is characteristic of ephedrine. Methcathinone (ephedrine), which was first synthesized in 1928, is the original designer drug derived from cathinone 
        • Clinical features include sympathomimetic activity and psychotic behavior (e.g., paranoia, hallucinations, and self- destructive and aggressive behavior) 
        • The core triad of symptoms (sudden development of altered mental status, agitated behavior, and autonomic dysfunction) was first described by Bell in 1849 in a study of psychiatric patients. Over the years, the syndrome consisting of these three symptoms has been referred to by many other names (e.g., Bell’s mania, acute exhaustive mania, delirious mania, lethal catatonia, agitated delirium, and excited delirium), but it is most accurately categorized as a subset of excitable malignant catatonia. 
        • Management
          •  In patients with cathinone-induced delirium, as in those with malignant catatonia, initial sedation should be achieved with the use of γ-aminobutyric acid type A (GABAA) agonists such as benzodiazepines or propofol. To minimize or prevent the worsening pyrexia and autonomic instability that occurs with the use of dopamine antagonists in such pa- tients, an agent such as intravenous haloperidol should be administered judiciously and only after therapy with GABAA agonists is initiated. Mono- therapy with dopamine antagonists should be avoided because it may exacerbate the catechol- amine surge and hyperthermia that often occur in patients with cathinone-induced delirium and thus cause the development of the malignant catatonia that is characteristic of the neuroleptic malignant syndrome 

Management of acute psychotic patient Case 40-2013:
  • sedate this patient with a parenteral benzodiazepine, which usually has a mild effect on the blood pressure 
  • If moderate doses of a benzodiazepine do not control the agitation, the airway should be secured through endotracheal intubation 
Differential Diagnosis Case 6-2012 (HIV/Toxoplasmosis)
  • Somnolence may result from abnormalities in 
    • the bilateral cortexes, 
    • reticular activating system (rostral brain stem), or 
    • bilateral medial thalami. 
  • Slow speech and difficulty putting words together may be indicative of 
    • aphasia due to dominant frontal-lobe or temporal-lobe dysfunction or could represent bradyphrenia, which may be caused by global, diffuse subcortical, extrapyramidal, or psychiatric dysfunction
    • Alternatively, difficulty putting words together could represent impaired attention resulting from global dysfunction, lesions in the prefrontal cortex, parietal lesions, or a psychiatric cause. 
  • Conversational repetition could be explained by impaired attention or by short-term memory impairment, attributable to the medial temporal lobe and limbic circuits (thalamus, mammillary bodies, and their connections) 
  • Slurred speech or dysarthria may be due to lesions in the corticobulbar tract, brain-stem motor nuclei, cranial nerves, cerebellum, extrapyramidal system, or vocal cords. 
  • Anisocoria with the right pupil larger than the left pupil suggests dysfunction of the right pupillary constrictor muscles, the parasympathetic component of the right oculomotor nerve, or the left sympathetic pathway. Often can be due to mass effect 
Differential Diagnosis of a Rapid Cognitive Decline: five major syndromes: Case 6-2012 (HIV/Toxoplasmosis)
  • hepatic encephalopathy, 
  • Wernicke’s encephalopathy, 
  • alcohol withdrawal, 
  • occult seizures, and 
  • infection 
Delirium as a cause of acute psychosis Case 5-2012 (HIV/TB/Cotard's Disease)
  • Psychosis is common in patients with delirium.
  •  The clinical diagnosis of delirium hinges on the presence of two cardinal features: 
    • disruption of attention and 
    • disruption of the sleep–wake cycle, which leads to fluctuation in symptoms over the course of a day 
  • A delirium can be easily missed if ancillary features such as psychosis overshadow the core problem of inattention 
  • An electroen- cephalogram (EEG) that shows diffuse slowing is suggestive of a delirium, but as in this patient, a normal EEG is not sensitive enough to reliably rule out a delirium 
  • DDx includes the following
    • HIV: 
      • HIV dementia: typical presentation is a progressive dementia with subcortical features (apathy, inattention, and loss of retentive memo- ry) and abnormalities of motor function, such as psychomotor slowing 
      • HIV Mania
      • HIV psychosis: sudden onset without prodrome, delusions (87% of patients), hallucinations (61%), and mood symptoms (81%)