Pathophysiology Like most animal tissues, brain
etabolism
depends primarily on glucose for fuel in most circumstances. A limited amount of
glucose can be derived from
lycogen
stored in
astrocytes, but it is consumed within minutes. For most practical purposes,
the brain is dependent on a continual supply of glucose diffusing from the blood
into the interstitial tissue within the
central nervous system and into the
eurons
themselves.
Therefore, if the amount of glucose supplied by the blood falls, the brain is
one of the first organs affected. In most people, subtle reduction of mental
efficiency can be observed when the glucose falls below 65 mg/dl (3.6 mM).
Impairment of action and judgement usually becomes obvious below 40 mg/dl (2.2
mM). eizures
may occur as the glucose falls further. As blood glucose levels fall below 10
mg/dl (0.55 mM), most neurons become electrically silent and nonfunctional,
resulting in coma. These brain effects are collectively referred to as
neuroglycopenia.
The importance of an adequate supply of glucose to the brain is apparent from
the number of nervous, hormonal and metabolic responses to a falling glucose
level. Most of these are defensive or adaptive, tending to raise the blood sugar
via
glycogenolysis and
gluconeogenesis or provide alternative fuels. If the blood sugar level falls
too low the liver converts a storage of glycogen into glucose and releases it
into the bloodstream, to prevent the person going in to a
diabetic coma, for a short period of time.
Brief or mild hypoglycemia produces no lasting effects on the brain, though
it can temporarily alter brain responses to additional hypoglycemia. Prolonged,
severe hypoglycemia can produce lasting damage of a wide range. This can include
impairment of cognitive function, motor control, or even consciousness. The
likelihood of permanent brain damage from any given instance of severe
hypoglycemia is difficult to estimate, and depends on a multitude of factors
such as age, recent blood and brain glucose experience, concurrent problems such
as hypoxia, and availability of alternative fuels. The vast majority of
symptomatic hypoglycemic episodes result in no detectable permanent harm.
Signs and symptoms Hypoglycemic symptoms and manifestations can be divided into those produced
by the counterregulatory hormones (pinephrine/adrenaline
and glucagon) triggered by the falling glucose, and the neuroglycopenic effects
Adrenergic manifestations
- Shakiness, anxiety, nervousness, tremor
-
Palpitations,
tachycardia
-
Sweating, feeling of warmth
- Pallor, coldness, clamminess
- Dilated
pupils
- Feeling of numbness "ins
and needles" in the fingers
Glucagon manifestations
- unger,
borborygmus
- ausea,
vomiting,
abdominal discomfort
-
Headache
(feeling of being hung-over)
Neuroglycopenic manifestations
- Abnormal mentation, impaired judgement
- Nonspecific dysphoria,
nxiety,
moodiness, depression, crying
- Negativism, irritability, belligerence, combativeness,
rage
-
Personality change, emotional lability
-
Fatigue, weakness, apathy,
lethargy, daydreaming,
leep
- Confusion,
mnesia,
dizziness,
delirium
- Staring, "glassy" look, blurred vision,
ouble
vision
- Automatic behavior, also known as
automatism
- Difficulty speaking, slurred speech
- taxia,
incoordination, sometimes mistaken for "runkenness"
- Focal or general motor deficit,
aralysis,
hemiparesis
-
Paresthesia,
eadache
- Stupor, coma, abnormal breathing
- Generalized or focal
eizures
Not all of the above manifestations occur in every case of hypoglycemia.
There is no consistent order to the appearance of the symptoms, if symptoms even
occur. Specific manifestations may vary by age and by severity of the
hypoglycemia. In young children, vomiting can sometimes accompany morning
hypoglycemia with
ketosis. In older children and adults, moderately severe hypoglycemia can
resemble ania,
mental illness,
drug intoxication, or drunkenness. In the elderly, hypoglycemia can produce
focal troke-like
effects or a hard-to-define malaise. The symptoms of a single person may be
similar from episode to episode, but are not necessarily so and may be
influenced by the speed at which glucose levels are dropping, and previous
incidence.
In newborns, hypoglycemia can produce irritability, jitters,
myoclonic jerks,
yanosis,
respiratory distress,
apneic episodes, sweating,
hypothermia, somnolence,
ypotonia,
refusal to feed, and seizures or "spells". Hypoglycemia can resemble
sphyxia,
hypocalcemia,
sepsis, or
eart
failure.
In both young and old patients, the brain may habituate to low glucose
levels, with a reduction of noticeable symptoms despite neuroglycopenic
impairment. In insulin-dependent diabetic patients this phenomenon is termed
hypoglycemia unawareness and is a significant clinical problem when
improved
glycemic control is attempted. Another aspect of this phenomenon occurs in
type I glycogenosis, when chronic hypoglycemia before diagnosis may be
better tolerated than acute hypoglycemia after treatment is underway.
Nearly always, hypoglycemia severe enough to cause seizures or
unconsciousness can be reversed without obvious harm to the brain. Cases of
death or permanent neurological damage occurring with a single episode have
usually involved prolonged, untreated unconsciousness, interference with
breathing, severe concurrent disease, or some other type of vulnerability.
Nevertheless, brain damage or death has occasionally resulted from severe
hypoglycemia.
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