Cerebral. Concussion. Sequelae of head injury.
Cerebral concussion is the most frequent craniocerebral trauma. It presents with cerebral symptoms of transitory character, short lasting loss of consciousness and no focal neurological deficit. No morphological changes are found in the cerebral parenchyma.
Pathogenesis; of the cerebral concussion is associated with functional disorders in the activating ascending reticular formation of the brainstem, caused by the traumatic vibration, which elicits temporary dysfunction in its associations with the cortex of the cerebral hemispheres. All this causes consciousness impairment, lasting from seconds to minutes and even more in some exceptional cases. The pathogenesis of cerebral concussion is also related to the development of brain edema, caused by transitory vasoparesis and higher vascular permeability.
Clinical features; are presented by entirely by cerebral symptomatology - the so called commotio syndrome characterised by;
- Loss of consciousness is short within seconds or several minutes due to temporary interruption of impulse transmission from the brain stem reticular formation to the cerebral cortex. Usual complaints include somnolence, fatigue, emotional and vegetative instability which are transitory.
- Amnesia. Immediately after consciousness recovery amnesia is possible. Retrograde and anterograde amnesia is shortlasting and covers a period of 1 or 2 hours.
- Headache; present in almost all patients with cerebral concussion and has mild to moderate intensity. The headache deteriorates with physical and mental loading. Usually the headache starts from the occiput and gradually engulfs the entire head. Patients complain that their head is being tightened by a helmet. Nausea, vomiting and dizziness are also commonly present.
- Vegetative syndrome; characterised by transitory autonomic disorders - most often paroxysmal bradycardia or tachycardia, orthostatic hypotension or arterial blood pressure fluctuations, perspiration, face reddening or getting pale.
- Psychic syndrome; psychomotor agitation and rare deliric states
- Mild focal neurological symptomatology; rarely seen and it involves anisocoria, mild nystagm, anisoreflexia.
- The patients frequently report subjective complaints, such as vertigo, dizziness while walking, fainting in getting up, tinnitus.
Diagnosis
- Neuroimaging studies (CT and MRI) do not display any pathological deviations.
- EEG can provide data of mild alpha rhythm suppression.
- Diagnosis made on typical clinical complaints
- Patient should be monitored for 24 hrs
Treatment
- Hospitalization is not needed for mild forms.
- Patients should keep bed rest regimen for 7 to 14 days and avoid the intake of excitatory substances (alcohol, coffee, coke, smoking, etc.)
- Medication therapy includes; analgesics, anti-emetics if required. Provided if there is drowsiness or astenia after the trauma, nootropics, such as Piracetam.