bubble_chart Overview

Concussion is a clinical syndrome caused by grade I brain injury, characterized by a brief loss of consciousness after head trauma, followed by rapid recovery. Apart from retrograde amnesia, there are no neurological deficits.

bubble_chart Pathological Changes

It was long believed that concussion was merely a temporary functional disorder of the central nervous system, with no visible organic damage, and no pathological changes were found in gross anatomy or histopathology. The transient inhibition of brain function observed may be related to factors such as molecular disturbances in brain cells caused by trauma, blockage of nerve conduction, dysregulation of cerebral blood circulation, damage to interneurons, and cerebrospinal fluid shock waves in the midline ventricles.

In modern times, electrophysiological studies of the nervous system suggest that damage to the brainstem reticular formation, affecting the function of the ascending activating system, is a key factor in causing consciousness disorders. However, these theories still cannot satisfactorily explain all phenomena associated with concussion, such as cases of fatal concussion, chronic brain atrophy and even dementia in professional boxers, as well as reports of grade I brain dysfunction in amateur boxers. Meanwhile, animal experiments have revealed that nerve cells in areas subjected to trauma exhibit mitochondrial swelling and displacement, neuronal axon swelling, and interstitial edema under electron microscopy. Biochemical studies have found that after concussion, not only do acetylcholine levels in the cerebrospinal fluid rise and potassium ion concentrations increase, but many enzyme systems affecting axonal conduction or brain cell metabolism also become disordered, leading to secondary damage.

Recently, new clinical observations have also shown that half of patients with mild concussion exhibit organic damage in brainstem auditory evoked potentials. Jeret (1993) conducted a prospective study, performing CT scans on 712 consecutive cases of minor closed head injury patients with a GCS score of 15, and found that 9.6% had acute injury lesions. Thus, concussion can no longer be summarized as "merely a transient brain dysfunction without definitive organic damage." With the continuous advancement and discoveries in medical science, the diagnostic term "concussion" will inevitably be imbued with new meanings.

bubble_chart Clinical Manifestations

After a craniocerebral injury, a brief loss of consciousness occurs immediately, lasting from several minutes to over ten minutes, generally not exceeding half an hour. However, occasionally, some patients may exhibit momentary confusion or daze without unconsciousness; in rare cases, prolonged unconsciousness or even death may occur, possibly due to the transmission of force through deep brain structures affecting vital centers such as the brainstem and medulla oblongata. When subjected to external force, patients experience not only a temporary disruption of cerebral and upper brainstem function but also inhibition of the lower brainstem, medulla oblongata, and cervical spinal cord. This leads to disturbances in the vasomotor and autonomic regulatory centers, causing a series of reactions such as slowed heart rate, decreased blood pressure, pale complexion, cold sweating, respiratory arrest followed by shallow and weak breathing, and limp limbs. In most reversible grade I concussion patients, central nervous system function rapidly recovers from the bottom up, progressing from the cervical spinal cord to the medulla oblongata, brainstem, and finally the cerebral cortex. In irreversible severe concussions, however, the inhibitory process may occur from the top down, causing prolonged dysfunction of the medullary respiratory and circulatory centers, leading to death.

After regaining consciousness, patients often experience symptoms such as headache, nausea, vomiting, vertigo, photophobia, and lack of strength, frequently accompanied by significant anterograde amnesia (retrograde amnesia), meaning they cannot recall events before and after the injury. The more severe the concussion and the longer the duration of primary unconsciousness, the more pronounced the anterograde amnesia becomes, though past memories remain unaffected.

During the convalescence stage of concussion, patients often exhibit symptoms such as dizziness, headache, nausea, vomiting, tinnitus, and insomnia. These symptoms typically gradually subside over several weeks to months. However, some patients may experience prolonged dizziness, headache, insomnia, dysphoria, difficulty concentrating, and memory decline. While some of these symptoms may belong to the convalescence stage, if no significant improvement occurs after 3 to 6 months, a thorough examination and analysis should be conducted to rule out delayed damage, in addition to considering psychological factors. Avoid hastily attributing these symptoms to "post-concussion syndrome," as this may unnecessarily increase the patient's psychological burden.

bubble_chart Diagnosis

The diagnosis of concussion was traditionally based on a history of injury, brief post-traumatic unconsciousness, recent memory loss, and the absence of positive neurological signs. However, there remains no reliable objective diagnostic criterion or clinical method to differentiate it from grade I cerebral contusion. Therefore, various auxiliary examinations are often required to confirm the diagnosis: - Skull X-rays show no fracture. - Lumbar puncture reveals normal intracranial pressure and cerebrospinal fluid without red blood cells. - Electroencephalography (EEG) may display low- to high-amplitude fast waves, occasionally with diffuse delta and theta waves, which resolve within 1–2 days. A minority of patients exhibit scattered slow waves that normalize within 1–2 weeks. - Brainstem auditory evoked potentials (BAEPs) may show prolonged interpeak latencies between waves I–IV, delayed latency of wave V, reduced amplitude, or waveform disappearance. - CT scans (both plain and contrast-enhanced) should yield negative results. However, clinicians should note that a small number of patients may initially present with negative CT findings but later develop delayed secondary intracranial lesions during continuous dynamic observation. Additionally, some researchers have reported using radioactive isotopes ¹²³

I-IMP and ^99mTc-HM-PAO for single-photon emission computed tomography (SPECT) scans in adolescent concussion patients, finding reduced blood flow in the cerebellum and occipital lobe in 70% of cases.

bubble_chart Treatment Measures

Concussion does not require special treatment. Generally, only 5–7 days of bed rest is needed, along with analgesic and sedative medications to alleviate symptoms, reducing external stimuli, and providing explanations to eliminate the patient's fear of concussion. Most patients recover within two weeks with a good prognosis. However, a small number of patients may develop secondary intracranial lesions or other complications. Therefore, during symptomatic treatment, close monitoring of the patient's mental state, level of consciousness, clinical symptoms, and vital signs is essential, and necessary examinations should be conducted promptly as needed. Avoid using morphine-like drugs that may interfere with observation. It is preferable to choose analgesics and sedatives with fewer side effects, such as Rotundine, Ibuprofen, Naproxen, Diazepam, bromides, Chlordiazepoxide, and Oryzanol to improve autonomic nerve function, as well as calcium channel blockers like Nimodipine.