Diffuse axonal injury

diffuse axonal injury

1. DIFFUSE AXONAL INJURY DR.Kalakoti chandra sekhar reddy

2. A form of post-traumatic brain injury which occurs over a  broad swath of myelinated tracts of the CNS, resulting in significant neurologic effects  ranging from loss of consciousness to  persistent vegetative state. Defnition

3. Diffuse axonal injury - Occurs in 50% of severely head injured patients and accounts for 35% of all death from Head injury. Triad - Lesion in corpus callosum. - Dorsolateral quadrant of brain stem. - Axonal rolling of white matter.

4. The susceptibility of axons to mechanical injury appears to be due to both their viscoelastic properties and their high organization in white matter tracts.

5. Two basic mechanisms -contact injuries -Inertial injuries physical stretch, or mechanoporation at the time of injury, results in damage to the axolemma and related axoplasm at the injured node of Ranvier Pathophysiology:

6. Either following impact or from impulse loading Brain lags behind due to inertia Movement away from skull cause low pressure [ tensile strain] - contrecoup injuries Strain within parenchyma cause diffuse injuries [concussions and DAI], tissue tear hemorrhages. Inertial injuries – acceleration/deceleration injuries

7. Pathogenesis of DAI - Four Stages Stage I: Axonal membrane injury and alteration in Ionic fluxes - axonal strain of 5% causes temporary failure in the generation and propagation of action potentials. There is increase in cytosolic free Ca2++. However ionic alterations are restored. Stage II: Reversible cytoskeletal damage. - Axonal strain > 5 - 10% - Axonal varicosities but not axonal disconnection. Stage III: Secondary axotomy - Strain is 15-20% - Induction of transient structural micro defect in cell membrane. - Increased Ca2+ in mitochondrial matrix - mitochondrial failure - lack of energy - impaired homeostasis - increases calcium influx - (Mechanoporation).

8. Stage IV: - Primary axotomy - Strain is > 20% - Most severe form - Tearing of axons

9. Axonal swelling in corpus callosum Disruption& globular swelling of axons in fornix. Dilated axonal spheroids in thalamus. Diffuse Axonal injury (DAI) Focal axonal swelling without disconnection ( Bodian silver) Dystrophic changes in cortical neurons proximal to damage Normal Axons in white matter Neurofilament immunostain

10. grade I:  involves grey-white matter interfaces most commonly: parasagittal regions of frontal lobes, periventricular temporal lobes less commonly: parietal and occipital lobes, internal and external capsules, and cerebellum often inapparent on conventional imaging may have changes on MR spectroscopy (MRS) grade II:  involves corpus callosum in addition to grade I locations observed in approximately 20% of patients most commonly: posterior body and splenium but does advance anteriorly with increasing severity of injury most frequently unilateral grade III:  involves brainstem in addition to grade I and II locations most commonly: rostral midbrain, superior cerebellar peduncles, medial lemnisci and corticospinal tracts Adams grading of DAI:

11. Grading of DAI: [ Gennarelli et al 1982] I. Microscopic axonal damage in the white matter, corpus callosum , brain stem or cerebellum without any macroscopic evidence. II. Macroscopic or Microscopic detected focal lesions in the CC and diffuse axonal damage. III. Macroscopic or microscopic injury, focal injury to CC + dorsolateral quadrant of rostral brain stem.

12. Wakefulness and alertness-RAS Swallowing -9,10,12 nerves Breathing –Apneustic center Arrhythmias-Chemoreceptor trigger zone Vision impairement:MLF and PPRF Brain stem dysfunction:

13. The amount of axonal injury in the brainstem is predictive of long-term vegetative state, supratentorial injury can result in focal neurological or neuropsychiatric deficits

14. MILD :coma for 6 to 24 hrs MODERATE :coma for more than 24 hrs but no clinical sign of brainstem dysfunction. SEVERE :more than 24 hrs with brainstem signs DAI:

15. Injury depends on rate and magnitude of acceleration Acceleration injury No injury subdural hematomas DAI Short duration longer duration high magnitude Well damped falls, assaults motor vehicle accidents

16. Transient reversible dysfunction due to trauma Loss of consciousness < 6 hours ,confusion, easy distractibility, amnesia Angular or horizontal acceleration deforming deeper aspects of the brain No permanent structural damage unless repeated Precise location of the functional derangement remains undetermined Diffuse brain injury - concussion

17. The outcome of patients after DAI has been linked to the number of lesions identified through imaging. Volume of the lesions and Location of lesion MRI is the imaging modality of choice as it identifies the lesions not identified on CT.

18. Study conducted by Marleen Maria van Eijck et,al

19. Paroxysmal autonomic instability with dystonia (PAID) appears to be a unique syndrome following brain injury. elevated temperature (≥ 38.5°C), Tachycardia (≥ 130 beats per minute), Tachypnoea (≥ 140 breaths per minute), Agitation Diaphoresis and Dystonia (rigidity or decerebrate posturing). The duration of an episode is cyclic, with at least one cycle per day for at least three days. PAID syndrome:

20. Managed with Antipyretics Morphine Benzodiazepines Betablockers

21. ICP measurement multimodality monitoring (MMM) PbtO 2  and cerebral microdialysis are independent markers of mortality. Management:

22. Main goal to prevent secondary brain injury like cerebral ischemia, intracranial hypertension, and energy dysfunction. P atient and  P athology  T argeted  ICP C are

23. Includes serial neurological examinations, imaging studies, ICP analysis, and measurements from other bedside physiologic monitors. MMM:

24. MMM can be used in evaluating adequate hyperventilation, osmotherapy, glycemic control, transfusion, CPP augmentation, therapeutic temperature modulation, and oxygen-based therapies

25. Pt with GCS <8 Motor posturing on presentation Abnormal ct on admission Age >40 1 episode of BP <90mm of hg In decompressive craniectomy following delayed surgery or failed medical management Indications of Icp monitoring

26. Invasive methods: Epidural catheter Intraparenchymal Intraventricular Non invasive: Mri based indirect icp measurement Optic nerve diameter measurement Icp monitoring techniques:

27. elevating the patients head to 30° hyperventilation only to a pCO 2  level of 25 mmHg Mannitol effect seen in 10-20 mins Barbiturates only for barbiturate induced coma last resort Treatment:

28. EVD Decompression VP shunt Surrgical management:

29. Thank you