Advertisement

Intensive Care Medicine

, Volume 6, Issue 3, pp 169–177 | Cite as

The activity of the sympathetic nervous system following severe head injury

  • Heide Hörtnagl
  • Alfons F. Hammerle
  • Johann M. Hackl
  • Thomas Brücke
  • Erik Rumpl
  • Helmut Hörtnagl
Original Articles

Abstract

The activity of the sympathetic nervous system during the course of severe closed head injury has been evaluated in 15 patients by measuring plasma levels of epinephrine and norepinephrine. With the onset of the transition stage from midbrain syndrome to the apallic syndrome the plasma levels mainly of norepinephrine started to increase and remained high during the further course of the disease. During the remission from the apallic syndrome the elevated norepinephrine levels started to decline. The data indicate that a longlasting overactivity of the sympathetic nervous system is a characteristic feature in the course of severe head injury.

As a rational therapy to protect the peripheral tissues against the consequences of a longlasting sympathetic overactivity we suggest the use of β-adrenergic blocking agents and adrenergic neuron blocking drugs.

Key words

Head injury Sympathetic nervous system Catecholamines Adrenergic beta receptor blockers Isoquinolines (debrisoquine) 

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Avenarius HJ, Gerstenbrand F (1977) The transition stage from midbrain syndrome to traumatic apallic syndrome. In: Dalle Ore G, Gerstenbrand F, Lücking CH, Peters G, Peters UH (eds) The Apallic Syndrome. Psychiatry series 14. Springer, Berlin Heidelberg New York, pp. 22–25Google Scholar
  2. 2.
    Batstone GF, Alberti KGMM, Hinks L, Smythe P, Laing JE, Ward CM, Ely DW, Bloom SR (1976) Metabolic studies in subjects following thermal injury. Intermediary metabolites, hormones and tissue oxygenation. Burns 2:207Google Scholar
  3. 3.
    Burch GE, Meyers R, Abildskov JA (1954) A new electrocardiographic pattern observed in cerebrovascular accidents. Circulation 9:719Google Scholar
  4. 4.
    Burch GE, Colcolough H, Giles T (1970) Intracranial lesions and the heart. Am Heart J 80:574Google Scholar
  5. 5.
    Cameron SJ, Doig A (1970) Cerebellar tumors presenting with clinical features of phaeochromocytoma. Lancet 1:492Google Scholar
  6. 6.
    Carruthers ME, Taggert P, Salpekar PD, Gatt JA (1976) Some metabolic effects of β-blockade on temperature regulation and in the presence of trauma. In: Schweizer W (ed) Beta-blockers: present status and future prospects. Huber, Bern, pp. 259–268Google Scholar
  7. 7.
    Cheng TO, Bashour TT (1976) Striking electrocardiographic changes associated with paeochromocytoma. Masquerading as ischemic heart disease. Chest 70:397Google Scholar
  8. 8.
    Connor RCR (1968) Heart damage associated with intracranial lesions. Br Med J 3:29Google Scholar
  9. 9.
    Cushing H (1902) Some experimental and clinical observations concerning states of intracranial tension. Am J Med Sci 124:375Google Scholar
  10. 10.
    Estanol BV, Marin OSM (1975) Cardiac arrhythmias and sudden death in subarachnoid haemorrhage. Stroke 6:382Google Scholar
  11. 11.
    Evans CH, Westfall V, Atuk N (1972) Astrocytoma mimicking the feature of phaeochromocytoma. N Engl J Med 289:1397Google Scholar
  12. 12.
    Falsetti HL, Moody RA (1966) Electrocardiographic changes in head injuries. Dis Chest 49:420Google Scholar
  13. 13.
    Fentz V, Gormsen J (1962) Electrocardiographic patterns in patients with cerebrovascular accidents. Circulation 25:22Google Scholar
  14. 14.
    Gerstenbrand F (1977) The symptomatology of the apallic syndrome. In: Dalle-Ore G, Gerstenbrand F, Lücking CH, Peters G, Peters UH (eds) The Apallic Syndrome. Psychiatry Series 14. Springer, Berlin Heidelberg New York, pp. 14–21Google Scholar
  15. 15.
    Gerstenbrand F, Lücking CH (1970) Die akuten traumatischen Hirnstammschäden. Arch Psychiat Nervenkr 213:264Google Scholar
  16. 16.
    Gobiet W, Werner U, Hackenberg K (1976) Verlaufsuntersuchungen zum Verhalten der Hormone des Hypophysenvorderlappens, der Nebennieren sowie der biogenen Amine nach schwerem Schädel-Hirn-Trauma. In: Schmidt K, Pottoff PC (eds) Neurogener Schock. Schattauer, Stuttgart, pp. 91–98Google Scholar
  17. 17.
    Goldman MR, Rogers EL, Rogers MC (1975) Subarachnoid haemorrhage: Association with unusual electrocardiographic changes. Jama 234:957Google Scholar
  18. 18.
    Haider W, Lackner F, Schlick W, Benzer H, Gerstenbrand F, Irsigler K, Korn A, Krystof G, Mayrhofer O (1975) Metabolic changes in the course of severe acute brain damage. Eur J Intens Care Med 1:19Google Scholar
  19. 19.
    Haider W, Benzer H, Krystof G, Lackner F, Mayrhofer O, Steinbereithner K, Irsigler K, Korn A, Schlick W, Binder H, Gerstenbrand F (1975) Urinary catecholamine excretion and thyroid hormone blood level in the course of severe acute brain damage. Eur J Intens Care Med 1:115Google Scholar
  20. 20.
    Hersch C (1961) Electrocardiographic changes in head injuries. Circulation 23:853Google Scholar
  21. 21.
    Hersch C (1964) Electrocardiographic changes in subarachnoid haemorrhage, meningitis and intracranial spaceoccupying lesions. Br Heart J 26:785Google Scholar
  22. 22.
    Hörtnagl H, Benedict CR, Grahame-Smith DG, McGrath B (1977) A sensitive radioenzymatic assay for adrenaline and noradrenaline in plasma. Br J Clin Pharmacol 4:553Google Scholar
  23. 23.
    Ingvar DH, Brun A (1972) Das komplette apallische Syndrom. Arch. Psychiat Nervenkr 215:219Google Scholar
  24. 24.
    Jäätelä A, Alko A, Avikainen Y, Karaharju E, Kataja J, Lakdensun M, Lepistö P, Rokkanen P, Tervo T (1975) Plasma catecholamines in severely injured patients: a prospective study on 45 patients with multiple injuries. Br J Surg 62:177Google Scholar
  25. 25.
    Lake CR, Ziegler MC, Kopin IJ (1976) Use of plasma catecholamine for evaluation of sympathetic neuronal function. Life Sci 18:1315Google Scholar
  26. 26.
    Landsberg L, Young JB (1978) Fasting, feeding and regulation of the sympathetic nervous system. N Engl J Med 298:1295Google Scholar
  27. 27.
    Mazey RM, Kotchen TA, Ernst CB (1974) A syndrome resembling phaeochromocytoma following a stroke. Jama 230:575Google Scholar
  28. 28.
    McNealy De, Plum F (1962) Brainstem dysfunction with supratentorial mass lesions. Arch Neurol 7:16Google Scholar
  29. 29.
    Menon IS (1964) Electrocardiographic changes simulating myocardial infarction in cerebrovascular accident. Lancet 2:433Google Scholar
  30. 30.
    Miller R, Stark DCC, Gitlow SE (1976) Paroxysmal hyperadrenergic state. A case during surgery for intracranial aneurysm. Anaesthesia 31:743Google Scholar
  31. 31.
    Nathan MA, Reis DJ (1975) Fulminating arterial hypertension with pulmonary edema from release of adreno-medullary catecholamines after lesions of the anterior hypothalamus in the rat. Circ Res 37:226Google Scholar
  32. 32.
    Pedersen EB, Christensen NJ (1975) Catecholamines in plasma and urine in patients with essential hypertension determined by double-isotope derivative technique. Acta Med Scand 198:373Google Scholar
  33. 33.
    Plum F, Posner JB (1966) Diagnosis of Stupor and Coma. First edition. F. A. Davis Company, PhiladelphiaGoogle Scholar
  34. 34.
    Reichenbach DD, Benditt ED (1970) Catecholamine and cardiomyopathy: The pathogenesis and potential importance of myofibrillar degeneration. Human Pathol 1:125Google Scholar
  35. 35.
    Sayer WJ, Moser M, Mattingly TW (1954) Phaeochromocytoma and the abnormal electrocardiogram. Am Heart J 48:42Google Scholar
  36. 36.
    Schuster S (1960) Electrocardiogram in subarachnoid haemorrhage. Br Heart J 22:316Google Scholar
  37. 37.
    Srivastavo SC, Robson AO (1964) Electrocardiographic abnormalities associated with subarachnoid haemorrhage. Lancet 2:431Google Scholar
  38. 38.
    Wilmore DW, Long JM, Mason AD, Shreen RW, Pruitt BA (1974) Catecholamines: Mediator of the hypermetabolic response to thermal injury. Ann Surg 180:653Google Scholar
  39. 39.
    Young JB, Landsberg L (1977) Stimulation of the sympathetic nervous system during sucrose feeding. Nature 269:615Google Scholar

Copyright information

© Springer-Verlag 1980

Authors and Affiliations

  • Heide Hörtnagl
    • 1
    • 5
  • Alfons F. Hammerle
    • 1
  • Johann M. Hackl
    • 2
  • Thomas Brücke
    • 1
  • Erik Rumpl
    • 3
  • Helmut Hörtnagl
    • 4
  1. 1.Department of PharmacologyUniversity of InnsbruckInnsbruckAustria
  2. 2.Department of AnaesthesiologyUniversity of InnsbruckInnsbruckAustria
  3. 3.Department of NeurologyUniversity of InnsbruckInnsbruckAustria
  4. 4.Department of Internal MedicineUniversity of InnsbruckInnsbruckAustria
  5. 5.Institut für Biochemische PharmakologieViennaAustria

Personalised recommendations