4. Clinical Presentation
Central syndromes
• Cerebral haemorrhage - those consequences following bleeding within the
cerebral structures
• Cerebral infarction
• Central encephalopathy, including hypoxic encephalopathy, that is,
alteration in neuronal function due to loss or diminution of oxygen supply
• Convulsions
• Movement disorders, including Parkinsonism and other disorders of
normal movement derived from central causes, whether added
movements, modulation of normal movement, attenuation of normal
movement, or loss of control of normal movement
Cerebellar syndromes
5. Clinical Presentation
Cranial nerve and related disorders
• Specific cranial nerve involvement, including speech and articulation disorders
• Ocular neurology
• Cochleo-vestibular neural disorders
• Synaesthesia
Autonomic syndromes
• Complex regional pain syndromes (CRPS) including Causalgia and reflex
sympathetic dystrophy (RSD)
• Postural hypotension – and other disturbances of autonomic function
• Cerebral salt wasting – this may be endocrinological in origin, however also
mediated by neural influence on the hypothalamus and pituitary gland.
6. Clinical Presentation
Spinal cord disorders
• Transverse myelopathy
• Amyotrophic lateral sclerosis (ALS), and other motor neurone disorders - the loss
of function of neural pathways controlling movement, in this case involving
specific neurones in the anterior horn of the spinal cord. The generic “motor
neurone disorder” includes more specific disorders such as ALS
• Spinal origin dystonia
Paralyses
• Keraunoparalysis (a transient syndrome, lasting a small number of hours. It is
seen in a limb in the line of current passage, and is thought to be due to vascular
spasm to the region. The limb becomes cold, blanched, numb, and pulseless, and
is confused with a compartment syndrome)
• Paraplegia and quadriplegia
8. Pathophysiology
• Direct electrical damage
• Thermal damage
• Tissue separation - by force or by electrostatic effects
• Ischemic changes
• Circulating neurohumoural actions
9. Pathophysiology of Delayed Syndrome
• Chronic ischaemia
• DNA / protein alteration that affect vascular endothelial cells, leading
to decreased blood supply to the central nervous system
(Ghosh et al., 1995a). Farrell and Starr (1968)
10. Pathology
• Focal petechial haemorrhages – especially in the cerebrum and medulla, and also
in the anterior horn grey matter of the spinal cord. He says these are more
common after AC shocks, and also large vascular tears are seen after lightning
injury.
• Chromatolysis – especially in pyramidal cells of the medullary nuclei, in anterior
horn cells, and the Purkinje cells of the cerebellum. These changes are said to be
patchy and sharply demarcated.
• “Curious” dilatation of perivascular spaces, which he suggests are due to gas
release, being seen largely in legal electrocution.
• Tortuosity and fragmentation of the axons of peripheral nerves with breakdown
of Schwann sheaths. Infiltration of the epineurium is seen with endothelial cells.
• Spiral-like changes in muscle fibres.
• In severe injury, the “entire brain and parts of the cord may be swollen softened
and even diffluent.”
11. Treatment
• Antidepresants
• Anti neuropathic pain
• Potential agents:
- Nitric oxide antagonists, glutamate antagonists, cortisol antagonists,
and antioxidants.
Andrews CJ, Reisner AD. Neurological and neuropsychological consequences of electrical and lightning shock:
review and theories of causation. Neural regeneration research. 2017 May;12(5):677.
12. Summary
• Lightning and electrical injuries often cause neurological symptoms
• Immediate vs delayed symptoms
• From CNS to PNS symptoms
REFERENCE:
Andrews CJ, Reisner AD. Neurological and neuropsychological consequences of electrical and lightning shock:
review and theories of causation. Neural regeneration research. 2017 May;12(5):677.
