Signs and symptoms postanoxic encephalopathy

Unconsciousness, bradycardia, hypotension and sweating, and is always followed by retrograde or post-traumatic (antegrade) amnesia, temporary lethargy, irritabihty and cognitive dysfunction. Muscles are flaccid, pupils are dilated and unreacting, pulse is weak and slow, and respiration is shallow.

Severity of concussion: it is given in table 13.3.

Findings: gross and light microscopic changes in the brain are usually absent, but biochemical and ultrastructural changes—mitochondrial ATP depletion, local disruption of blood-brain barrier occur. CT and MRI scans are usually normal.

Differentiation 13.2: drunkenness and concussion


S. No.

Feature

Drunkenness

Concussion

1.

Skin

Flushed, congested and warm

Pale, cold and sweating

postanoxic encephalopathy

2.

Pulse

Rapid and bounding

Slow and feeble

3.

Pupils

Dilated; contracted in coma

Contracted in pontine hemorrhage

4.

Light reflex

Sluggish

May be brisk

5.

Respiration

Sighs, puffs, eructates

Shallow, irregular, slow

6.

Memory

Confused, disoriented

Retrograde amnesia, unrelieved by time

7.

Behavior

Uncooperative, abusive, talkative, sulky

Quiet and retracted, curled up in bed, photophobia

8.

Urine/blood

Examination will be helpful

Retention of urine, urine may contain albumin

9.

History

History of having consumed alcohol, smell of alcohol

History of head injury with features of concussion

Table 13.3: concussion (ji. KIiikj sc, iio

Grade 1

Grade 2

1 grades

Transient confusion

Transient confusion

No loss of consciousness

No loss of consciousness

postanoxic encephalopathy

Briefer prolonged loss of consciousness

Concussion symptoms or mental status

Concussion symptoms or mental status

Change resolves in 15 min

J

Post-traumatic automatism: it is intimately associated with amnesia. After an accident, the patient may speak and act in a purposive manner, but does not remember anything later on. Retrograde amnesia: loss of memory preceding the event. Anterograde amnesia: loss of memory subsequent to the event that caused the amnesia.

Post-concussion syndrome: seen in patients who returned to work too early after head injury. It consists of headache, vertigo, lassitude, irritability and depression which may persist for months.

Second impact syndrome is characterized by rapid death due to a second concussion prior to a return to baseline functioning after an initial one.Postanoxic encephalopathy

Punch drunk syndrome (dementia pugiiistica or boxer’s encephaiopathy): A condition occurring late in boxer’s career or years after retirement which is the cumulative result of recurrent cerebral concussions.

Signs and symptoms: there may be deterioration of speed and reflexes, and incoordination along with personality change associated with social instability and sometimes paranoia and delusions. Later, memory loss progresses to full dementia, often associated with parkinsonian signs, ataxia or intention tremors, shuffling, broad-based gait and dysarthria.

Autopsy: chronic SDH, attenuation of corpus callosum, DAI and cortical atrophy may be seen.

Tliere are four forms of diffuse TBI: axonal injury, vascular injury, hypoxic ischemic encephalopathy and brain swelling.Postanoxic encephalopathy these categories overlap and they are often accompanied by various forms of focal TBI.

Literature: forensic medicine and toxicology.

TABLE 3-20: signs and symptoms of hyponatremia

Symptom severity correlates both with the magnitude and rapidity of the fall in serum na” concentration

Gastrointestinal complaints include anorexia, nausea, and vomiting

Headaches, muscle cramps, and weakness also occur early

Altered sensorium with impaired response to verbal and painful stimuh, inappropriate behavior, auditory and visual hallucinations, asterixis and obtnndation can be seen

Severe or acute hyponatremia

Seizures, or decorticate/decerebrate posturing develop

Bradycardia and hyper – or hypotension can occur

postanoxic encephalopathy

Respiratory arrest and coma may result

• central nervous system pathology is due to cerebral edema and symptoms result from a failure in cerebral adaptation

When plasma osmolality falls acutely, osmotic equilibrium is maintained by

Extrusion of intracellular solutes

Influx of water into brain

Neurologic symptoms result when osmotic equilibrium is achieved by water influx into brain cells

If solute extrusion is successful and osmotic equilibrium maintained, cell swelling is minimized

Na” extrusion from the brain by na-K” atpase and na channels is the first pathway activated (minutes)

Persistent hyperosmolality activates K” channels, which lead to K” extrusion (hours)

TABLE 3-21: neurologic injury from hyponatremia

postanoxic encephalopathy

Neurologic injury from hyponatremia is secondary to either hyponatremie encephalopathy or improper therapy (too rapid or overcorrection)

Greater than 90% of cases of neurologic injury are secondary to hyponatremie encephalopathy

Hypoxia is the major factor causing neurologic injury

Blunts RVD, an ATP-dependent active ion transport process, which allows na” accumulation in the brain and cerebral edema

Major stimulns for AVP secretion enhancing water entry into neurons

Respiratory arrest and seizures occur suddenly in hyponatremie encephalopathy and are associated with permanent neurologic injury

• predictive factors include young age, premenopausal state, female sex, and encephalopathy; hypoxia as a result of respiratory arrest or seizure reduces RVD, which in turn exacerbates cerebral edema and often induces permanent neurologic injury

postanoxic encephalopathy

Premenopausal womeu are at 25-fold iucreased risk for permanent neurologic iujury

RVD may be decreased in young women (estrogen and progesterone inhibit brain na”’-K”’ atpase)

• AVP concentration is higher in women and AVP decreases brain ATP in women but not men

TABLE 3-21: (continued)

Chronic hyponatremia is characterized by fewer and milder neurologic symptoms

• regulatory mechanisms promote organic osmolyte (glutamate, taurine, and myoinositol) loss from brain

Abbreviations: RVD, regulatory voliune decrease; ATP, adenosine triphosphate; AVP, arginine vasopressin

Literature: lange instant access.

Unconsciousness, bradycardia, hypotension and sweating, and is always followed by retrograde or post-traumatic (antegrade) amnesia, temporary lethargy, irritabihty and cognitive dysfunction.Postanoxic encephalopathy muscles are flaccid, pupils are dilated and unreacting, pulse is weak and slow, and respiration is shallow.

Severity of concussion: it is given in table 13.3.

Findings: gross and light microscopic changes in the brain are usually absent, but biochemical and ultrastructural changes—mitochondrial ATP depletion, local disruption of blood-brain barrier occur. CT and MRI scans are usually normal.

Differentiation 13.2: drunkenness and concussion

S. No.

Feature

Drunkenness

Concussion

1.

Skin

Flushed, congested and warm

Pale, cold and sweating

2.

Pulse

Rapid and bounding

Slow and feeble

3.

Pupils

Dilated; contracted in coma

Contracted in pontine hemorrhage

4.

Light reflex

Sluggish

May be brisk

5.

Respiration

Sighs, puffs, eructates

postanoxic encephalopathy

Shallow, irregular, slow

6.

Memory

Confused, disoriented

Retrograde amnesia, unrelieved by time

7.

Behavior

Uncooperative, abusive, talkative, sulky

Quiet and retracted, curled up in bed, photophobia

8.

Urine/blood

Examination will be helpful

Retention of urine, urine may contain albumin

9.

History

History of having consumed alcohol, smell of alcohol

History of head injury with features of concussion

Table 13.3: ( oik ussion (jiudiik) sc ulo

Grade 1

Grade 2

1 grades

Transient confusion

Transient confusion

No loss of consciousness

No loss of consciousness

Briefer prolonged loss of consciousness

Concussion symptoms or mental status

Concussion symptoms or mental status

Change resolves in 15 min

J

Post-traumatic automatism: it is intimately associated with amnesia.Postanoxic encephalopathy after an accident, the patient may speak and act in a purposive manner, but does not remember anything later on.

Retrograde amnesia: loss of memory preceding the event.

Anterograde amnesia: loss of memory subsequent to the event that caused the amnesia.

Post-concussion syndrome: seen in patients who returned to work too early after head injury. It consists of headache, vertigo, lassitude, irritability and depression which may persist for months.

Second impact syndrome is characterized by rapid death due to a second concussion prior to a return to baseline functioning after an initial one.

Punch drunk syndrome (dementia pugiiistica or boxer’s encephaiopathy): A condition occurring late in boxer’s career or years after retirement which is the cumulative result of recurrent cerebral concussions.Postanoxic encephalopathy

Signs and symptoms: there may be deterioration of speed and reflexes, and incoordination along with personality change associated with social instability and sometimes paranoia and delusions. Later, memory loss progresses to full dementia, often associated with parkinsonian signs, ataxia or intention tremors, shuffling, broad-based gait and dysarthria.

Autopsy: chronic SDH, attenuation of corpus callosum, DAI and cortical atrophy may be seen.

Tliere are four forms of diffuse TBI: axonal injury, vascular injury, hypoxic ischemic encephalopathy and brain swelling. These categories overlap and they are often accompanied by various forms of focal TBI.

Literature: review of forensic medicine and toxicology.Postanoxic encephalopathy