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A clinical form of traumatic brain injury; confusion and other acute symptoms do not require an observed loss of consciousness. Alcohol intoxication can coexist with the injury.^[ref][ref]

Neither the smell of alcohol nor a drunken appearance excludes concussion or a more serious head injury. The useful distinction comes from the history, a complete examination and repeated assessment; alcohol intoxication and head injury may occur together.

First establish the order of events. Witnesses may describe drinking followed by progressive slurring, unsteadiness and drowsiness, or a blow or fall followed immediately by altered consciousness, confusion or a gap in human memory. Ask about the amount and timing of the drink, the mechanism of injury and any interval of apparent recovery. A person may have fallen because of alcohol intoxication, and subsequently have suffered a head injury. Conversely, an injured person may be mistakenly described as drunk because of slurred speech and an unsteady gait.

Examine the level of consciousness, orientation, speech, human memory and ability to follow commands. In alcohol intoxication, disinhibition, slurred speech, incoordination, vomiting and increasing drowsiness can occur; severe poisoning can progress to coma and impaired breathing. After concussion, confusion, amnesia, headache, dizziness, nausea and vomiting may occur, with or without an observed loss of consciousness. Thus vomiting or drowsiness alone does not decide the diagnosis.^[ref][ref]

Look for a scalp wound, swelling or other evidence of impact, and examine the pupils, their reaction to light, limb movements and any focal neurological deficit. Unequal pupils, one-sided weakness, a worsening level of consciousness or a seizure should prompt concern for significant traumatic brain injury, rather than be dismissed as ordinary drunkenness or uncomplicated concussion. The absence of an external wound does not exclude an internal injury. Nor are a flushed face, a particular pulse or the smell of drink sufficiently specific to settle the question.

The defensible diagnostic conclusion may initially be uncertainty requiring observation and investigation. Current guidance specifically requires important traumatic brain injury to be excluded before depressed consciousness is attributed to intoxication. Modern computed tomography and measurement of blood glucose can resolve problems that an 1864 bedside examination could not; these are later diagnostic aids, not equipment to attribute to the examination's period.^[ref]

General paresis combines progressive mental deterioration with a characteristic disorder of speech, fine movement and motor control. The historical phrase “general paralysis of the insane” does not mean complete, simultaneous immobility of every muscle.

Early changes may include impaired judgment, forgetfulness, altered personality, irritability, inappropriate confidence and loss of ordinary social restraint. Expansive or grandiose delusions are characteristic in some cases, but depression, suspiciousness or less spectacular cognitive failure can occur. Increasing dementia and reduced insight are more fundamental than any one extravagant belief.

The physical examination may disclose hesitating or slurred articulation, tremulous lips and tongue, facial tremor, deteriorating handwriting and impaired coordination of the hands. Gait becomes unsteady and weakness advances. Unequal or abnormally reacting pupils, altered reflexes and seizures may occur. Later disease can bring severe cognitive incapacity, swallowing difficulty, incontinence and dependence. Mental and motor manifestations need not develop in a fixed order or with equal severity.^[ref]

The name general paresis was already advocated in a January 1864 pathological study to avoid the ambiguity of “general paralysis.”^[ref] Modern medicine recognises the classical disease as a form of neurosyphilis, involving chronic injury to the brain. This causal diagnosis should be separated from the historical clinical label; it was not securely established by the wording of an 1864 examination. Syphilis serology, relevant cerebrospinal fluid findings and exclusion of alternative causes now help establish the diagnosis.^[ref]

Several mimics deserve explicit comparison. Mania can resemble the expansive mental phase, and depression or psychotic illness can resemble other presentations, but a sustained progressive combination of cognitive decline, characteristic speech disturbance and neurological signs argues for organic disease. Alcohol intoxication can produce tremor, slurred speech and an unsteady gait; an acute time course or improvement with clearance differs from progressive general paresis, although chronic alcohol-related disease may complicate the distinction. Other dementias, chronic cerebral vascular disease, tumours and some toxic or metabolic disorders can likewise combine cognitive and motor abnormalities.

A focal stroke generally gives a more abrupt and lateralised deficit; a series of strokes can produce a stepwise course. Parkinsonism can impair speech and gait but has a different predominant motor pattern. Tabes dorsalis can produce marked sensory ataxia, absent tendon reflexes and bladder disturbance with relatively preserved intellect; it can also coexist with paretic disease. The diagnosis rests on the pattern, course and corroborating investigation, not on grandiosity or a tremulous tongue alone.^[ref]