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SPINAL AND PERIPHERAL
NERVE POISONS
BY PRIYANKA ( MBBS STUDENT )
STRYCHNOS NUX-VOMICA (KUCHILA)
Loganiaceae family.
The ripe fruit contains seeds which are poisonous.
They are flat, circular discs, 2.5 × 0.6 cm, slightly concave on one side and
convex on the other, ash grey in color, have a shiny surface and are covered
with silky hairs.
They look like enlarged RBCs.
Unbroken seeds are not poisonous, as the hard pericarp is not soluble in digestive
juices.
ACTIVE PRINCIPLES
i. Strychnine—Alkaloid
ii. Brucine—Alkaloid
iii. Loganin—Glucoside
PROPERTIES OF
STRYCHNINE
Colorless
Bitter
odorless
rhombic prism-shaped crystals
Dissolves sparingly in water or ether
dissolves well in alcohol and benzene
USES
It is used as a
 respiratory stimulant
 rodenticide
 for killing stray dogs
 herbal and homeopathic remedies
 purgative
 appetite suppressant
 a constituent of nerve tonics.
 It can be found as an adulterant in some street drugs
 (cocaine, heroin and amphetamines).
ACTIONS
Strychnine competitively antagonizes the inhibitory neurotransmitter glycine by
blocking its post-synaptic uptake by brainstem and spinal cord receptors
The inhibiting effect of glycine is reduced and nerve impulses are triggered with
lower levels of neurotransmitters.
There is no inhibitory effect, the motor neurons do not stop their stimulus and the victim
will have constant muscle contractions
Its action is particularly in the anterior horn cells (especially in Renshaw cells of the
spinal cord).
GABA, the neurotransmitter for presynaptic inhibitory neurons is not affected by
strychnine
SIGNS & SYMPTOMS
A 'conscious' seizure is the characteristic presentation of strychnine poisoning.
Bitter taste
Choking sensation in throat and stiffness of the neck and face.
Prodromal symptoms: Restlessness, increased acuity of perception, increased rigidity of muscles
and muscular twitchings.
Face: Cyanosed, look is anxious, eyes are staring, eyeballs are prominent and the pupils are dilated.
Mouth is filled with bloodstained froth.
Convulsions: The threshold for CNS stimulation is lowered with the result that any sensory stimulus
(pain, touch or noise) may produce violent muscular spasm.
Initially, clonic but eventually become tonic and affect all the muscles at the same time.
SIGNS & SYMPTOMS CONTD.
Risus sardonicus results from contraction of the jaw and facial muscles in which the
corners of the mouth are drawn back.
Convulsions are most marked in anti-gravity muscles resulting in hyperextension
(opisthotonus)
Sometimes, the spasm of the abdominal muscles may bend the body forward
(emprosthotonus) or sideways (pleurosthotonus).
Duration of convulsions is about half to 2 min.
In between convulsions, muscles are completely relaxed. Patient looks well, but exhausted
and breathing is resumed.
After 5-15 min, on the slightest impulse, like sudden noise, current of air or on gently
touching the patient, another convulsion occurs.
SIGNS & SYMPTOMS
CONTD.
Increased muscle tone, hyperreflexia, agitation, restlessness and
convulsions lead to
lacticacidosis
rhabomyolysis
hyperthermia.
Death occurs within 4-5 convulsions as the patient cannot breathe.
Consciousness is not lost and the mind remains clear till death.
Death is due to medullary paralysis or asphyxia due to spasm of
respiratory muscles or due to exhaustion.
FATALITY
Fatal dose
• Strychnine: 15-50 mg (1-2 mg/kg body wt).
• 1 crushed seed.
Fatal period: 1-2 h.
DIFFERENTIAL DIAGNOSIS:
 Tetanus
 Epilepsy
 Hysteria
 Neuroleptic malignant syndrome
 Malignant Hyperthermia
 Stimulant use.
TREATMENT
There is no antidote for strychnine poisoning.
Maintain clear airway and adequate ventilation.
Control of convulsions: Dark room, free from noise and disturbance.
Benzodiazepines remain the first-line of treatment for strychnine induced muscular hyperactivity.
Diazepam 0.1-0.5 mg/kg IV slowly.
If ineffective, general anesthetics and/or muscle relaxants, like gallamine should be given.
Barbiturates, like pentobarbital sodium or sodium amytal are antidotes. Dose: 300-600 mg IV.
Gastric lavage with KMnO4 may be done cautiously, if there are no convulsions. Activated
charcoal is recommended as it adsorbs strychnine and may reduce its absorption if given 1 h of
ingestion.
Hyperthermia is treated by active cooling with ice water immersion, cooling blanket or mist and
fan.
Symptomatic treatment.
PMF
i. Not characteristic.
ii. Rigor mortis appears early.
iii. Signs of asphyxia.
iv. Extravasated blood may be found in the muscles.
v. Viscera are congested.
Death is usually accidental due to overdose, quack remedies and
poison
mistaken for some other harmless drug, or in children eating the seeds.
It is used as an aphrodisiac, as cattle and arrow poison and to kill
dogs and rats.
Differentiation 53.1:
PERIPHERAL NERVE POISONS
 Alkaloid
 Peripheral muscle relaxant
 Available from the plant Chondrodendron
tomentosum or some species of Strychnos
plants
Curare
ACTIVE PRINCIPLES
 d-tubocurarine
 dimethyl tubocurarine
 syncurine
 succinylcholine chloride.
ACTION
 It blocks the postsynaptic nicotinic acetylcholine receptors in the
muscles
 Thus causing flaccid paralysis of skeletal muscles.
SIGNS AND SYMPTOMS
 paralysis of voluntary muscles
 followed by paralysis of respiratory muscles resulting in death
from asphyxia.
 The mind remains clear till the end.
Fatal dose: 30-60 mg of curarine parenterally.
Fatal period: 1-2 h.
TREATMENT
 Artificial respiration and O2 should be given.
 If applied to a wound or introduced by an arrow, a ligature should be
applied proximal to the site and is washed with a solution of KMnO4.
 Atropine 0.6-1.2 mg, followed by physostigmine (1-2 mg, physiological
antidote) or neostigmine (0.5- 1 mg) subcutaneously should be given.
PMF
 Those of asphyxia.
 Skin and tissue from the wound due to the arrow or injection
should be preserved.
MLI
 Most deaths are from its use in anesthesia.
 It is also used as arrow poison.
CONIUM MACULATUM (HEMLOCK)
 spotted hemlock
 because of the purple spots on its stem
 All parts of the plant are poisonous
 whole plant has a mousy odor which is intensified by crushing
the leaves or stems.
ACTIVE PRINCIPLES
 Coniine, methyl coniine and six other alkaloids.
 Coniine content is highest in the unripe fruit and seeds.
ACTIONS
 It causes paralysis of the motor nerve terminals in the muscles,
gradually spreading to the motor cells of the spinal cord and the brain.
SIGNS & SYMPTOMS
Nausea, unpleasant mousy odor in breath.
Ingestion causes
burning in the mouth and throat
gastric inflammation
vomiting, diarrhea
slow respiration and pulse
mental confusion
tremors
blindness.
This is followed by progressive muscular paralysis due to depression of the motor nerves.
The lower limbs are affected first and the paralysis ascends till the muscles of
respiration are affected.
Delirium, convulsions and coma may supervene and the patient dies of asphyxia due to
respiratory paralysis. The mind remains clear till the end.
 Fatal dose: 60 mg coniine
 Fatal period: Few hours.
FATALITY
TREATMENT
i. Gastric lavage with KMnO4.
ii. Artificial respiration.
iii. Oxygen inhalation.
iv. Stimulants.
v. Symptomatic treatment.
PMF
 Those of asphyxia, the remains of the roots or leaves
should be looked for in the stomach contents and
preserved for chemical analysis.
MLI
 Poisoning is mostly accidental
THANK YOU!

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Spinal and peripheral nerve poisons quick review

  • 1. SPINAL AND PERIPHERAL NERVE POISONS BY PRIYANKA ( MBBS STUDENT )
  • 2. STRYCHNOS NUX-VOMICA (KUCHILA) Loganiaceae family. The ripe fruit contains seeds which are poisonous. They are flat, circular discs, 2.5 × 0.6 cm, slightly concave on one side and convex on the other, ash grey in color, have a shiny surface and are covered with silky hairs. They look like enlarged RBCs. Unbroken seeds are not poisonous, as the hard pericarp is not soluble in digestive juices.
  • 3.
  • 4. ACTIVE PRINCIPLES i. Strychnine—Alkaloid ii. Brucine—Alkaloid iii. Loganin—Glucoside
  • 5. PROPERTIES OF STRYCHNINE Colorless Bitter odorless rhombic prism-shaped crystals Dissolves sparingly in water or ether dissolves well in alcohol and benzene
  • 6. USES It is used as a  respiratory stimulant  rodenticide  for killing stray dogs  herbal and homeopathic remedies  purgative  appetite suppressant  a constituent of nerve tonics.  It can be found as an adulterant in some street drugs  (cocaine, heroin and amphetamines).
  • 7. ACTIONS Strychnine competitively antagonizes the inhibitory neurotransmitter glycine by blocking its post-synaptic uptake by brainstem and spinal cord receptors The inhibiting effect of glycine is reduced and nerve impulses are triggered with lower levels of neurotransmitters. There is no inhibitory effect, the motor neurons do not stop their stimulus and the victim will have constant muscle contractions Its action is particularly in the anterior horn cells (especially in Renshaw cells of the spinal cord). GABA, the neurotransmitter for presynaptic inhibitory neurons is not affected by strychnine
  • 8. SIGNS & SYMPTOMS A 'conscious' seizure is the characteristic presentation of strychnine poisoning. Bitter taste Choking sensation in throat and stiffness of the neck and face. Prodromal symptoms: Restlessness, increased acuity of perception, increased rigidity of muscles and muscular twitchings. Face: Cyanosed, look is anxious, eyes are staring, eyeballs are prominent and the pupils are dilated. Mouth is filled with bloodstained froth. Convulsions: The threshold for CNS stimulation is lowered with the result that any sensory stimulus (pain, touch or noise) may produce violent muscular spasm. Initially, clonic but eventually become tonic and affect all the muscles at the same time.
  • 9. SIGNS & SYMPTOMS CONTD. Risus sardonicus results from contraction of the jaw and facial muscles in which the corners of the mouth are drawn back. Convulsions are most marked in anti-gravity muscles resulting in hyperextension (opisthotonus) Sometimes, the spasm of the abdominal muscles may bend the body forward (emprosthotonus) or sideways (pleurosthotonus). Duration of convulsions is about half to 2 min. In between convulsions, muscles are completely relaxed. Patient looks well, but exhausted and breathing is resumed. After 5-15 min, on the slightest impulse, like sudden noise, current of air or on gently touching the patient, another convulsion occurs.
  • 10. SIGNS & SYMPTOMS CONTD. Increased muscle tone, hyperreflexia, agitation, restlessness and convulsions lead to lacticacidosis rhabomyolysis hyperthermia. Death occurs within 4-5 convulsions as the patient cannot breathe. Consciousness is not lost and the mind remains clear till death. Death is due to medullary paralysis or asphyxia due to spasm of respiratory muscles or due to exhaustion.
  • 11. FATALITY Fatal dose • Strychnine: 15-50 mg (1-2 mg/kg body wt). • 1 crushed seed. Fatal period: 1-2 h.
  • 12. DIFFERENTIAL DIAGNOSIS:  Tetanus  Epilepsy  Hysteria  Neuroleptic malignant syndrome  Malignant Hyperthermia  Stimulant use.
  • 13. TREATMENT There is no antidote for strychnine poisoning. Maintain clear airway and adequate ventilation. Control of convulsions: Dark room, free from noise and disturbance. Benzodiazepines remain the first-line of treatment for strychnine induced muscular hyperactivity. Diazepam 0.1-0.5 mg/kg IV slowly. If ineffective, general anesthetics and/or muscle relaxants, like gallamine should be given. Barbiturates, like pentobarbital sodium or sodium amytal are antidotes. Dose: 300-600 mg IV. Gastric lavage with KMnO4 may be done cautiously, if there are no convulsions. Activated charcoal is recommended as it adsorbs strychnine and may reduce its absorption if given 1 h of ingestion. Hyperthermia is treated by active cooling with ice water immersion, cooling blanket or mist and fan. Symptomatic treatment.
  • 14. PMF i. Not characteristic. ii. Rigor mortis appears early. iii. Signs of asphyxia. iv. Extravasated blood may be found in the muscles. v. Viscera are congested.
  • 15. Death is usually accidental due to overdose, quack remedies and poison mistaken for some other harmless drug, or in children eating the seeds. It is used as an aphrodisiac, as cattle and arrow poison and to kill dogs and rats. Differentiation 53.1:
  • 17.  Alkaloid  Peripheral muscle relaxant  Available from the plant Chondrodendron tomentosum or some species of Strychnos plants Curare
  • 18.
  • 19. ACTIVE PRINCIPLES  d-tubocurarine  dimethyl tubocurarine  syncurine  succinylcholine chloride.
  • 20. ACTION  It blocks the postsynaptic nicotinic acetylcholine receptors in the muscles  Thus causing flaccid paralysis of skeletal muscles.
  • 21. SIGNS AND SYMPTOMS  paralysis of voluntary muscles  followed by paralysis of respiratory muscles resulting in death from asphyxia.  The mind remains clear till the end.
  • 22. Fatal dose: 30-60 mg of curarine parenterally. Fatal period: 1-2 h.
  • 23. TREATMENT  Artificial respiration and O2 should be given.  If applied to a wound or introduced by an arrow, a ligature should be applied proximal to the site and is washed with a solution of KMnO4.  Atropine 0.6-1.2 mg, followed by physostigmine (1-2 mg, physiological antidote) or neostigmine (0.5- 1 mg) subcutaneously should be given.
  • 24. PMF  Those of asphyxia.  Skin and tissue from the wound due to the arrow or injection should be preserved.
  • 25. MLI  Most deaths are from its use in anesthesia.  It is also used as arrow poison.
  • 26. CONIUM MACULATUM (HEMLOCK)  spotted hemlock  because of the purple spots on its stem  All parts of the plant are poisonous  whole plant has a mousy odor which is intensified by crushing the leaves or stems.
  • 27.
  • 28. ACTIVE PRINCIPLES  Coniine, methyl coniine and six other alkaloids.  Coniine content is highest in the unripe fruit and seeds.
  • 29. ACTIONS  It causes paralysis of the motor nerve terminals in the muscles, gradually spreading to the motor cells of the spinal cord and the brain.
  • 30. SIGNS & SYMPTOMS Nausea, unpleasant mousy odor in breath. Ingestion causes burning in the mouth and throat gastric inflammation vomiting, diarrhea slow respiration and pulse mental confusion tremors blindness. This is followed by progressive muscular paralysis due to depression of the motor nerves. The lower limbs are affected first and the paralysis ascends till the muscles of respiration are affected. Delirium, convulsions and coma may supervene and the patient dies of asphyxia due to respiratory paralysis. The mind remains clear till the end.
  • 31.  Fatal dose: 60 mg coniine  Fatal period: Few hours. FATALITY
  • 32. TREATMENT i. Gastric lavage with KMnO4. ii. Artificial respiration. iii. Oxygen inhalation. iv. Stimulants. v. Symptomatic treatment.
  • 33. PMF  Those of asphyxia, the remains of the roots or leaves should be looked for in the stomach contents and preserved for chemical analysis.
  • 34. MLI  Poisoning is mostly accidental