In Medical Articles

Case description:

A 20-year-old female with mild developmental delay and a life-long history of seizures starts experiencing better cognitive function and greatly reduced seizure activity after going on a strict low-carbohydrate diet.  Then she is in a violent auto collision in which she receives a clear neck/back injury but without perceived head trauma.  Two months later she experiences a dramatic spike in her seizure activity that never subsides and she loses her cognitive gain.  Imaging suggests a multifocal or generalized disorder of brain function.


Can cervical trauma without apparent blunt head injury aggravate epilepsy when there is a two-month delay in the increased seizure activity?


Medical research establishes that cervical trauma can affect brain function.   Cervical trauma can cause decreased proprioception.  Decreased proprioception can be a late affect of cervical trauma.  Reflex seizures can be precipitated by proprioception; the “Jacksonian” latency of epileptic symptoms is well known. Cervical trauma has been associated with hippocampal spiking. “Late seizures” manifest alterations in the hippocampus.  Temporal lobe epilepsy originates in the hippocampus.

Method of Study:

There appear to be no medical studies of the effect cervical trauma can have on epilepsy patients.  Perhaps there is no practical way to gather a meaningful test group of epilepsy patients who have experienced increased seizure activity after a cervical injury and compare them with epilepsy patients who have not had a cervical injury.  For now, causation studies will apparently have to be based on elements of medical science rather than through epidemiology.


Cervical trauma can affect brain function.  Both whiplash injury and concussion alter processing of the middle-latency somatosensory evoked potentials (SEP) component N60 in the acute post traumatic period.  The SEP similarities suggest that the overlapping clinical symptomatology post whiplash and concussion may reflect a similar underlying mechanism of rotational mild traumatic brain injury.1

Decreased blood flow to the brain also appears to be a factor.  There is an association between intraneural circulation and venous congestion. Compromise in intraneural circulation appears to be the first step in the pathophysiological cascade of nerve injury.  Mechanical or chemical stimuli that exceed the physical capabilities of neural tissues induce venous congestion, thereby impeding intraneural circulation and axoplasmic flow.2  Subsequent hypoxia and alterations in microvascular permeability cause an inflammatory response in nerve trunks and dorsal root ganglia that leads to subperineurial edema and increased endoneurial fluid pressure.3

Blood flow to the brain can directly affect brain function and health.  It is well-recognized that high blood pressure can lead to seizures.  A Swedish study of cervical whiplash associated disorders (WAD) patients investigated the resting state rCBF (regional cerebral blood flow) and altered rCBF and found that WAD patients had somatic symptoms, posttraumatic stress symptoms and personality traits that the control group did not have.   Compared with healthy controls, patients had heightened resting state rCBF bilaterally in the posterior parahippocampal and the posterior cingulate gyri in the right thalamus and the right medial prefrontal gyrus, as well as lowered tempero-occipital blood flow.  The altered rCBF in the patient group was correlated to neck disability ratings.  The indication was an involvement of the posterior cingulate, parahippocampal and medial prefrontal gyri.4

Blunt head trauma, or other force sufficient to traumatically injure the brain has been easily understood to disrupt brain function.  It has long been suggested that an association of cervical injury with brain damage should be investigated.

“It is matter of crucial importance that we investigate and manage the clinical problems of whiplash injuries in our patients not only with regard to the musculoskeletal system and peripheral nervous system but also with greater attention to the finer details of behavioral and neurological deficits.”5

Substantial medical research now supports that post-traumatic cervical WAD can have an adverse affect on brain function, including cognitive deficits.6  Decreased proprioception has been shown to be a factor, without head trauma or frank brain injury.  The whiplash motion itself does not necessarily cause traumatic brain injury.  Rather, the association appears to be the altered afferent stimulation from proprioceptors in the cervical spine.7  Control of body posture is integrated in the flocculus of the midcerebellum.  Alteration in visual pursuit movements, which are reflective of parietal lobe function, is related to abnormal input from the neck proprioceptors.8  

Post-traumatic whiplash syndrome can include cognitive disturbances as a consequence of altered cervical spine proprioception.  Injury to the facet proprioceptors may be undetectable in and of itself on standard medical examination, but the resulting disturbance of the brain is evident.9  Cervical spinal injuries can affect the body’s postural control system and proprioceptive activity, causing disturbed eye movement without any detectible pathologic change in the vestibular system or the central nervous system.10  Similarly, it has been shown that cognitive interpretation can be influenced by neck proprioceptive input and other changes in the interacting postural control system.11  The cognitive deficits from WAD can also have psychological consequences.12

            A particular study13 focused on WAD patients for whom structural damage could not be identified by MRI/CT, but who appeared to have delayed brain damage in the frontal regions.  The evidence supported causation of parieto-occipital hypoperfusion by activation of nociceptive afferents from the upper cervical spine.  Patients in the study  averaged below normal performance levels on tasks of divided attention and working memory.  There appeared to be a significant correlation between pain intensity, emotional-psychological factors, and cognition.

Reflex seizures –  seizures induced by stimuli in sensitive patients – have been recognized for over 100 years.14  The study of reflex seizures has evolved, especially in the last 40 years.15  The seizures are precipitated by integration of higher cortical function.  Proprioception – the unconscious perception of movement and spatial orientation arising from stimli within the body itself – is a well-established precipitator of reflex seizures.16  In fact, the Commission on Classification and Terminology of the International League Against Epilepsy offers a along list of precipitating stimuli for reflex seizures, including

Visual stimuli

Flickering light – color to be specified when possible


Other visual stimuli








Hot water


There can be a latency period from stimulus onset to the clinical event.  Cerebral lesions are often evident and may have occurred well before the onset of attacks.  Proprioceptive-induced seizures begin less suddenly and may have initial “Jacksonian sensory manifestations” that involve a progression of the location of the seizure in the brain, which leads to a “march” of the motor presentation of symptoms.17

In 1975, Chauvel and Lamarche elicited reflex seizures by stimuli that produced proprioceptive input to the hyperexcitable cortical area that demonstrated “the paramount role of proprioceptive afferents.”  Thus, seizures originally described as movement-induced are more accurately described as “proprioceptive-induced.”  These reflex seizures, although rare, are well-understood in current neurology.  They were thoroughly reviewed by Vignal and colleagues in 1998 and have been the topic of ongoing discussion.18

Decreased proprioception can be a late effect of WAD.  Medical studies support that such late effects can develop weeks, months, or years after the trauma.  The studies included concussion injuries as well as WAD, and include seizures as a resulting condition.

In 2003, Zifkin and Andermann concluded that patients with eating-induced epilepsy and extralimbic seizure onset were more sensitive to proprioceptive stimuli.4 In the case study that is the subject of this article, it seems relevant to note that the patient’s seizure activity decreased substantially in the months preceding her auto collision when she went on a strict low-carbohydrate diet.

Post-traumatic epilepsy (PTE) can involve the temporal lobe.  In a Russian study involving 161 patients with mild PTE, the localization of epileptic center was determined to be associated with a pathology in the neocortex.  The duration of latency period, clinical features, and prognosis in patients with mild and severe brain injury were similar.  The high frequency of seizures and long duration of epilepsy indicated a poor prognosis.19                                             

            The ultimate lesion to the brain may be in the hippocampus,20 the hallmark of many forms of temporal lobe epilepsy.21  Whiplash injuries have been directly associated with hippocampal spiking six to eight weeks after the trauma.  The growth and development of trauma-induced hippocampal spiking followed the classic sequence for the spread of an epileptogenic focus.22

            Seizures occurring months or years after injury are called “late seizures.”  Recurring “late seizures” make up the clinical syndrome of “posttraumatic epilepsy.”23  Animal studies demonstrate that PTE manifests alterations in the hippocampus.24   The risk of late seizures has been demonstrated to be from 26 to 53%.25  Young children are more prone to early seizures, and adolescents and adults are more prone to late seizures.26  PTE also was significantly correlated with a worse functional outcome one year after the trauma.27

PTE tends to lower the patient’s seizure threshold, to persist, and to result in a higher mortality rate than TBI without epilepsy.28


Principles of medical science are consistent with an association between cervical injury without blunt head trauma and an increase in the epilepsy patient’s seizure activity.



  1. Zumsteg D. Wennbera R. Gutlinq E. Hess K., Whiplash and concussion: similar acute changes in middle-latency SEPs. Krembil Neuroscience Centre, Toronto Western Hospital, University of Toronto, Toronto, ON, Canada.  Comment in: Can J Neurol Sci. 2007 Mav:34(‘2):260.
  2. Robert J. Nee and David Butler, Management of peripheral neuropathic pain: Integrating neurobiology, neurodynamics, and clinical evidence, Physical Therapy in Sport 7 (2006), p. 40 [citing Greening & Lynn, 1998; Hasue, 1993; Kobayashi, Yoshizawa, & Nakai, 2000; Lundborg & Dahlin, 1992; Ogata & Naito, 1986; Olmarker & Rydevik, 1991; Parke & Whalen, 2002; Rempel, Dahlin, & Lundborg, 1999; Rydevik, Brown, & Lundborg, 1984)]
  3. Robert J. Nee and David Butler, Management of peripheral neuropathic pain: Integrating neurobiology, neurodynamics, and clinical evidence, Physical Therapy in Sport 7 (2006), p. 40 [citing Hasue, 1993; Igarashi, Yabuki, Kikuchi, & Myers, 2005; Kobayashi et al., 2000; Lundborg, 1988; Lundborg, Myers, & Powell, 1983; Mackinnon, Dellon, Hudson, & Hunter, 1984; O’Brien et al., 1987; Parke & Whalen, 2002; Rempel et al., 1999; Rydevik, Myers, & Powell, 1989; Triano & Luttges, 1982; Yabuki, Onda, Kikuchi, & Myers, 2001)]
  4. Linnman C, Appel L, Soderlund A, Frans O , Engler H, Furmark T, Gordh T. Langstrom B. Fredrikson M., Department of Psychology, Uppsala University, Box 1225, SE-751 42 Uppsala Sweden. Chronic whiplash symptoms are related to altered regional cerebral blood flow in the resting state.  EurJPain. 2009 Jan;13(1):65-70. Epub 2008 May 16.
  5. Ommaya AK, Faas F, Yarnel P: Whiplash injury and brain damage: an experimental study.  JAMA. 1968 Apr 22; 204(4): 285-9.
  6. Bogdan P. Radanov, MD, Jiri Dvorak, MD, and Ladislav Valich, PhD, Cognitive Deficits in Patients after Soft Tissue Injury of the Cervical Spine, Department of Psychaitry, University of Bern, Switzerland, and the Department of Neurology, Wilhelm Schulthess Hospital, Zirich, Switzerland, accepted for publication October 10, 1990.
  7. Mallinson Al, Longridge NS: Dizziness from whiplash and head injury: differences between whiplash and head injury. Am J Otol. 1998 Nov; 19(6): 814-8.
  8. Tjell C, Rosenhall U: Smooth pursuit neck torsion test: a specific test for cervical dizziness. Am J Otol. 1998 Jan; 19(1): 76-81.
  9. Radanov. Dvorak and Valich: Cognitive Deficits in Patients after Soft Tissue Injury of the Cervical Spine, Spine 1992, Feb. 17 (2): 127-131
  10. Gimse R, Tjell C, Bjorgen IA, Sauntte C: Disturbed eye movements after whiplash due to injuries to the posture control system. J Clin Exp Neuorpsychol. 1996 Apr; 18 (2): 178-8. Heikkila HV, Wenngren BI:  Cervicocephalic kinesthetic sensibility, active range of cervical motion, and oculomotor function in patients with whiplash injury. Arch Phys Med Rehabil. 1998 Sep; 79(9): 1089-94.
  11. Gimse R, Tjell C, Bjorgen IA, Tyssedal JS, Bo K. Reduced cognitive function in a group of whiplash patients with demonstrated disturbances in the posture control system. J Clin Exp Neuorpsychol. 1997 Dec; 19(6): 838-49
  12. Alexander MP: In the pursuit of proof of brain damage after whiplash injury. Neurology. 1998 Aug; 51(2): 336-40.
  13. Radanov BP, Bicik I, Dvorak J, Antinnes J, Von Schulthess GK, Buck A. Relation between neuropsychological and neuroimaging findings in patients with late whiplash syndrome. J Neurol Neurosurg Psychiatry. 1999 Apr; 66(4): 485-9.
  14. Gowers WR, Epilepsy and other chronic convulsive diseases: their causes, synptoms and treatment. London: JA Churchill, 1901
  15. Feriha Ozer, Aytul Mutlu, Tufan Ozkayran, Haseki Education and Research Hospital, Neurology Clinic, Istanbul, Turkey, Epileptic Disorders Vol. 5, No. 3, September 2003
  16. Chauvel P, Lamarche M. Analyze d’une ches un singe porteur d’un foyer rolandique.  Neurochirurgie 1975; 21: 121-37
  17. Benajmin G. Zifkin and Frederick Andermann, Precipitating Stimuli for Reflex Seizures, Epileptic Discord, 2003; 5: 165-8
  18. Vignal JP, Biraben A, Chauvel PY, Reutens DC. Reflex partial seizures of sensorimotor cortex (including cortical reflex myoclonus and startle epilepsy). In: Zifkin BG, Andermann F, Beaumanoir A, Rowan A, editors. Reflex epilepsies and reflex seizures. Advances in Neurology; vol 75. Philadelphia: Lippincott-Raven; 1998:207-26.
  19. Kotov AS. Belova lu A. Posttraumatic epilepsy: the theory and the practice.  Zh Nevrol Psikhiatr Im S S Korsakova, 2010:110 (3 Suppl 2):48-51.  [Article in Russian]
  20. Kharatishvili I. Nissinen JP, Mclntosh TK. Pitkanen A. Epilepsy Research Laboratory, A. 1. Virtanen Institute for Molecular Sciences, University of Kuopio, and Department of Neuroiogy, Kuopio University Hospital, Finland: A model of posttraumatic epilepsy induced by lateral fluid-percussion brain injury in rats.  Neuroscience. 2006 Jun 30;140(2):685-97.
  21. Golarai G, Greenwood AC, Feeney DM, Connor JA. Department of Neurosciences, University of New Mexico: Physiological and structural evidence for hippocampal involvement in persistent seizure susceptibility after traumatic brain injury. J Neuroscience, 2001 Nov 1;21(21):8523-37.
  22. Liu YK. Chandran KB. Heath RG. Unterharnscheidt F: Subcortical EEG changes in rhesus monkeys following experimental hyperextension-hyperflexion (whiplash).  Spine, 1984 May-Jun;9(4):329-38.
  23. Pagni CA, Zenqa F. Neurosurgical Clinic University of Torino, Torino, Italy. Posttraumatic epilepsy with special emphasis on prophylaxis and prevention.  Acta Neurochir Suppl, 2005;93:27-34.
  24. Pitkanen A. Immonen RJ. Grohn OH. Kharatishvili I. Epilepsy Research Group, Department of Neurobiology, A. I. Virtanen Institute for Molecular Sciences, University of Kuopio, Kucpic, Finland. From traumatic brain injury to posttraumatic epilepsy: what animal models tell us about the process and treatment options.  Epilepsia, 2009 Feb;50 Suppl 2:21-9.
  25. Benardo LS. Department of Neurology, State University of New York Downstate Medical Center, Brooklyn, New York: Prevention of epilepsy after head trauma: do we need new drugs or a new approach?  Epilepsia, 2003:44 SuppI 10:27-33.
  26. Asikainen I. Kaste M. Sarna S. Department of Neurology, Kauniala Hospital, Kauniainen, Finland: Early and late posttraumatic seizures in traumatic brain injury rehabilitation patients: brain injury factors causing late seizures and influence of seizures on longterm outcome.  Epilepsia. 1999 May;40(5):584-9.
  27. Mazzini L. Cossa FM, Anqelino E. Campini R, Pastore I, Monaco F. Department of Neurology, San Giovanni Bosco Hospital, Torino, Italy. Posttraumatic epilepsy: neuroradiologic and neuropsychological assessment of long-term outcome.  Epilepsia. 2003 Apr;44(4):569-74.
  28. Kharatishvili I, Pitkanen A, Epilepsy Research Laboratory, Department of Neurobiology, A. I. Virtanen Institute for Molecular Sciences, University of Kuopio, Finland. Posttraumatic epilepsy.  Curr Qpin Neurol. 2010 Apr:23(2):183-8.