Refers to an alteration in mental status that affects the patients cognition or level of arousal.
It describes a clinical syndrome rather than a diagnosis and has many potential causes.
Broadly includes mental status changes due to focal or global brain insults, but the term most commonly is used to describe the latter.
Focal cognitive desert deficits such as aphasia or amnesia can mimic global encephalopathy syndrome.
A subtype of a cephalopathy includes delirium in which the patient has a cute altered mental status with waxing and waning attention.
The etiology and differential diagnosis of encephalopathic syndromes is determined by history of onset, progression of symptomatology, its total duration, physical examination including mental status examination, and laboratory/radiologic tests.
Encephalopathy time of onset includes categories: hyperacute, acute, subacute, chronic.
Encephalopathy occurring over anytime course can be due to systemic disease, or toxic-metabolic insult.
Hyperacute-onset encephalopathy leads to consideration of cerebrovascular disease, seizures, trauma, or migraines.
Hyper acute causes of encephalopathy includes intracranial hemorrhage, which is characterized by the compartment where the bleeding occurs: intracerebral, subarachnoid, subdural, or epidural spaces.
Subarachnoid hemorrhage, particularly when caused by ruptured cerebral aneurysm, is often associated with a sudden, severe headache, which can be accompanied by meningeal signs such as meningismus, photophobia, nausea, seizures and decreased level of arousal.
Intraparenchymal hemorrhage causes include: hypertension, cerebral amyloid angiopathy, head trauma, coagulopathy, brain metastases, and dural sinus thrombosis.
Epidural hematoma often occurs from damage to the middle meningeal artery, allowing arterial blood to collect in the epidural space leading to increased intracranial pressure and brain shift.
Acute-onset encephalopathy is considered for neurologic infections such as bacterial or viral meningitis or encephalitis, or acute demyelination.
Subacute-onset encephalopathy leads to consideration of neoplastic disease or metastases, autoimmune conditions, and infections.
Subdural hematoma can produce cognitive symptoms that emerge slowly, sometimes taking weeks after onset.
Brain tumors can cause encephalopathy as a result of direct infiltrative damage to local tissue, edema, mass effect, and intra-cranial shifts, with effects on intracranial pressure, seizures or hemorrhages.
Chronic-onset encephalopathy considers neurodegenerative conditions such as dementia.
Toxic and metabolic insults can cause variable onset of insult encephalopathy, dependent on the toxin/metabolite.
Ischemic stroke caused by lack of blood flow to one or more regions of the brain, leads to cerebral infarction.
Ischemic stroke clinical findings are related to the location of the ischemia/infarction, most patients present with focal defects.
Embolic strokes typically have an acute presentation with maximum symptoms at onset, whereas small vessel strokes, lacunar strokes, may have a stuttering pace over minutes to hours.
Global encephalopathy can occur with infarctions to certain regions of the brain including bilateral thalami, territories of the right middle and anterior cerebral arteries, and diffuse and bilaterally located small emboli.
Seizures are caused by abnormal, excessive, rhythmic electrical discharges in the brain.
Seizures usually occur as discreet events with a rapid onset, although clinical presentation is variable and depends on where in the brain the aberrant electrical activity originates and whether it remains in one location-that is partial, or becomes more widespread, that is generalized.
Generalized seizures Lead to a loss of consciousness and are followed by a period of global encephalopathy, known as a postictal state.
Partial seizures produce focal symptoms reflecting the function of the area where the aberrant electrical activity occurs-motor, sensory, autonomic-and can cause encephalopathy when the cognitive networks are involved.
Migraine is characterized by unilateral and throbbing headaches that last several hours and is often accompanied by nausea, photophobia, and phonophobia.
Migraine headaches tend to build over a course of minutes and maybe preceded by an aura that is often visual or somatosensory.
Migraine can produce symptoms of confusion in rare instances.
Traumatic brain injury is a common cause of hyperacute encephalopathy.
Concussion refers to mild Traumatic brain injury associated with altered mental status.
Patient with concussion can experience a posttraumatic encephalopathy as part of a broader postconcussive syndrome of headaches, dizziness, mental fogginess, intolerance of loud noises or bright lights, and the onset of symptoms may be delayed by hours or days following impact.
Neuropsychiatric symptoms may accompany the syndrome and include fatigue, sleepiness, insomnia, personality changes and slow processing speed.
Sudden onset encephalopathy can occur with hypertensive emergencies, metabolic derangement, medications, drug withdrawal, and other toxic exposures.
Psychiatric processes such as panic attacks, nonepileptic seizures, fugue state, and psychosis can also present as a sudden onset encephalopathy.
Psychiatric illness may cause acute mania, psychosis, panic, anxiety, and depression along with cognitive impairment, Catalonia, psychomotor agitation, or slowing.
Subdural hematoma, the slow accumulation of blood which may take days or even weeks can occur as a clinically significant mass effect and result in encephalopathy.
Subdural hematoma symptoms include: headache, impaired arousal, focal deficits, cognitive impairment, and seizures.
Subdural hematoma may be caused by head trauma, coagulopathies, anticoagulants, and intracranial hypotension.
Demyelinating disease of the CNS include multiple sclerosis and acute disseminated encephalitis and they may manifest as an encephalopathy.
CNS infection such as meningitis and encephalitis can present with acute encephalopathy, usually accompanied by headache and fever.
In transient global amnesia temporary loss of ability to form new memories and patients present with disorientation.
In transientt global amnesia the mental status exam is normal outside of short-term recall.
The process resolves within 24 hours and may be triggered by intense physiological or emotional stimuli.
Systemic conditions associated with acute encephalopathy include: systemic infections, systemic autoimmune diseases, metabolic disturbances, drugs or drug withdrawal, and toxin ingestions.