Ivan Mikula, Snježana Miškov, Ružica Negovetić and Vida Demarin
University Department of Neurology, Sestre milosrdnice University Hospital, Zagreb, Croatia
SUMMARY _ Visual evoked potentials (VEP) were studied in 30 patients with recent whiplash injury. VEP recordings were obtained from Oz, after stimulation with pattern reversal of full-field chessboard. Latencies (ms) and amplitudes (mV) of N70, P100 and N145 were measured. Recordings were obtained immediately upon admission, and then again three months and one year after the injury. The latencies of P100 and N145 were prolonged immediately after the injury, and even more so three months later, while the results obtained at one year showed no significant difference compared with those recorded at three months, suggesting the damage detected at three months to be definite. Study results indicated the visual system to be also affected by whiplash injury. The possible mechanisms resulting in the development of neural dysfunction initially show a fast-acting pattern, later assuming a slow-acting pattern. They mostly affect latencies and produce permanent changes. These characteristics correspond to demyelination, prolonged vascular insufficiency, or both.
Key words: Whiplash injuries, physiopathology; Whiplash injuries, diagnosis; Evoked potentials,visual;
Many traffic accident casualties suffer or claim to suffer from the consequences of whiplash injury. A whiplash injury can result from sudden acceleration or deceleration of the head and neck relative to the body. This mostly occurs in car accidents. During the accident, a sudden movement of the head and neck in one direction is followed by recoil in the opposite direction. Such whiplash-like movements are very forceful and may cause stretching of various structures with consequential microtraumas of intervertebral joints, ligaments, muscles, and nervous tissue. The injury may be even more severe if the neck was rotated during the accident. The sequels may range from mild headache or neck stiffness to the development of tetraparesis, incontinence, or serious psychologic problems. Most of these casualties proceed with law suits and demand financial compensation for their health problems, many of them upon the advice of their lawyers, friends, or even medical staff. As the diagnosis is mostly based on subjective symptoms and signs that can easily be simulated, many have recognized the situation as a way to get easy money. There is a great necessity to find a way to evaluate the consequences of whiplash injury in an objective manner, and to avoid manipulation from both parties involved1. The neuroradiologic methods show only structural changes2. Most symptoms, especially those of a late syndrome, are due to the dysfunction of specific neural pathways, with no detectable structural lesion, and can only be assessed by neurophysiologic methods. The most widely used neurophysiologic tests are EMG with SNCV and MNCV, and evoked potentials1,2. While the acute changes can mostly be explained by the neck sprain, the pathogenesis of the late syndrome is still unknown2,3.
We tried to evaluate the detectable dysfunction of the visual pathway involved in the development of the acute and late symptoms of whiplash injury, and to propose a hypothesis on the dysfunction development.
Measurements were performed in 30 patients (21 male and nine female, mean age 37±7.5 years) with recent (less than 30 days) whiplash injury, treated as outpatients at the Departments of Neurosurgery and of Neurology, Sestre milosrdnice University Hospital. All study subjects had been injured in traffic accidents. Their findings were compared with those obtained in a control group of 30 sex- and age-matched normal control subjects (21 male and nine female, mean age 38±9.7 years). The diagnosis of whiplash injury in the study patients was made according to the mechanism of trauma, i.e. sudden acceleration and deceleration of the head and (posterior) neck relative to the body. None of the patients had any serious somatic or psychiatric disease detectable by psychiatric examination, ECG, CBC, urea, creatinine, electrolytes, and ABS. None of the patients had any structural damage to the neural pathways detectable by the neuroradiologic methods used (x-ray, CT, MRI). EEG and TCD findings were normal. Ophthalmologic examination revealed no obvious damage to the visual system. The patients caught or suspected of malingering were automatically excluded from the study. Five patients failed to show up for control testing at three months, and two more dropped out after one year. Most of the study patients (85%) had received some physical therapy and symptomatic medication.
The latencies and amplitudes of the main components of visual evoked potentials (VEP) were compared between the patients with recent whiplash injury and normal controls. All recordings were obtained by use of a Medelec Sensor and analyzed on an Apple Mackintosh computer. Recordings were obtained immediately upon admission, and then again three months and one year after the injury.
VEP recordings were taken from Oz electrode with a reference linked to Cz, after stimulation with pattern reversal of the full-field chessboard, delivered by means of a B/W monitor. Latencies (ms) and amplitudes (mV) of N70, P100 and N145 were measured, with averaging of 256 runs.
Test results obtained in the patient and control group were compared by use of the Wilcoxon Mann-Whitney test.
The results of comparison of the latencies and amplitudes of the main VEP components between the patient group (all three measurements) and control group by use of the Wilcoxon Mann-Whitney test are presented in Tables 1 and 2, and Figures 1 and 2.
Table 1. Latencies (ms) of VEP components (N70, P100 and N145) in
the group of patients with recent whiplash injury (immediately upon
admission, at three months, and at one year after the injury) and in the
control group of normal subjects (statistically significant differences
indicated by asterisk)
Fig. 1. Latencies (ms) of VEP components (N70, P100 and N145) in the
group of patients with recent whiplash injury (immediately upon admission,
at three months, and at one year after the injury) and in the control
group of normal subjects (statistically significant differences indicated
by asterisk).
Fig. 2. Amplitudes (mV) of VEP components (N70, P100 and N145) in the group of patients with recent whiplash injury (immediately upon admission, at three months, and at one year after the injury) and in the control group of normal subjects (no statistically significant differences were observed).
Evoked potentials have proved to be sensitive indicators of subtle neurophysiologic changes in patients with whiplash injury, however, the findings reported in the literature vary. Most authors found an unilateral or bilateral increase in the latencies of auditive evoked potentials, i.e. interpeak latencies I-III or I-V, with no changes in the absolute latencies and V/I amplitude ratio, which persisted after six months3-6. As some earlier investigations have shown the vestibular system to remain relatively intact, while explaining the lack of coordination of eye movements and vertigo by lesion of the proprioceptive receptors in the neck7, these abnormalities could be supposed to be due to delayed changes involving the brainstem. The visual and somatosensory pathways as well as the cognitive response have been less thoroughly investigated and, although some disturbances have been reported, the findings appear to be even less decisive8,9.
Changes in the blood supply due to compression within the vertebrobasilar system might account for some of the abnormalities, since a correlation between these findings and asymmetry of MBFV in the left and right vertebral artery has been observed in these patients8,10. These findings have been supported by a group of authors who investigated SPECT and PET findings in these patients and found parieto-occipital hypoperfusion by relative quantification using SPECT and bicisate (Neurolite, ECD) followed by PET and F-18-fluorodeoxyglucose (FDG)11. The clearly prolonged latencies with no evident changes of amplitudes have also raised the question of possible demyelination as an underlying pathogenetic mechanism12,13.
Our previous results14,15 have shown that the visual system is not spared in the course of whiplash injury. The latencies of VEP components recorded in the group of patients with recent whiplash injury immediately upon admission showed significantly longer absolute latencies of P100 and N145 than those measured in normal control subjects (p<0.05). There were no significant differences in the amplitudes. While the first follow-up results obtained three months after the injury seemed to indicate a rather quick progression of dysfunction, the results recorded one year after the injury were found to have remained unchanged, showing no further progression. As no further deterioration was recorded by the end of the one-year period, it appeared that the three-month results could be considered definite. Thus, it could be concluded that the possible mechanisms leading to the development of neural dysfunction in the visual system are initially characterized by fast action, whereby it slows down, mostly affecting VEP latencies and producing permanent changes that do not improve within a year period. These characteristics correspond to demyelination, prolonged vascular insufficiency, or both.
Correspondence to: Ivan Mikula, M.D., Ph.D., University Department of Neurology, Sestre milosrdnice University Hospital, Vinogradska c. 29, HR-10000 Zagreb, Croatia
Received January 27, 2000, accepted February 15, 2000
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I. Mikula, S. Miškov, R. Negovetić i V. Demarin
Istraživanje vidnih evociranih potencijala (VEP) provedeno je u 30 ispitanika koji su pretrpjeli trzajnu ozljedu vratne kralježnice. Mjerenje VEP provedeno je s točke Oz, nakon stimulacije pomoću monitora sa svjetlećim šahovskim poljem, uz inverziju uzorka. Izmjerene su latencije (ms) i amplitude (mV) valova N70, P100 i N145. Mjerenja su obavljena odmah nakon prijma te ponovno tri mjeseca nakon ozljede. Latencije P100 i N145 bile su produljene odmah nakon ozljede, {to je bilo još izraženije nakon tri mjeseca. Mjerenja provedena godinu dana nakon ozljeđivanja nisu pokazala statistički značajnih razlika, ukazujući na to da su oštećenja zabilježena nakon tri mjeseca bila konačna. Rezultati ispitivanja ukazuju na to da pri trzajnoj ozljedi vratne kralježnice stradava i vidni put. Mogući mehanizam nastanka neuralne disfunkcije u početku je brz, a potom djeluje sporo, utječući pretežito na latencije evociranog odgovora i stvarajući trajne promjene. Ova obilježja odgovaraju demijelinizaciji, produženoj vaskularnoj insuficijenciji ili objema.
Ključne riječi: Trzajne ozljede, fiziopatologija; Trzajne ozljede,
dijagnostika; Evocirani potencijali, vidni
Acta clin Croat, Vol. 39, No. 1, 2000