This is an article by Britt Talley Daniel MD, member of the American Academy of Neurology, the American Headache Society, migraine textbook author, and blogger.

Acute Confusional Migraine (ACM) is the development of acute altered sensorium with confusion, irritability, drowsiness, nausea, or vomiting following mild non-concussive head injury.  It primarily affects only children and adolescents. 

Ten percent of school-aged children have migraine.  Out of the migraine group, one in six have acute confusional migraine.  It has been suggested that ACM is underdiagnosed also, and the actual occurrence rate may be higher. 

Although migraine has been studied since Hippocrates mentioned “sick headache” in 400 BC and Galen described “hemicrania” in AD 200, Acute Confusional Migraine is in the beginning stage of medical research. Few case studies appear in the medical literature. Researchers have recommended that ACMs be added to the official International Classification of Headache Disorders as a “migraine variant.”  This hasn’t happened yet, but writers of this opinion think unity with ICHD-3 may help pediatricians and others more easily recognize this type of migraine.

At times confusional migraine may occur spontaneously.  Most of the patients have throbbing headache when they recover enough to describe how they feel and go on to develop migraine later in life.  There is an increased history of migraine in the family of affected patients.

Tests such as CAT or MRI scan of the brain are normal although the EEG is typically slow during the attack and becomes normal after recovery.  The syndrome occurs mostly in young children or adolescents who remain amnestic for what happened after the event.  Occasional patients may have recurrent attacks.

Acute care physicians should have ACM in their differential diagnosis along with the other possible and more concerning neurologic diseases such as subdural, epidural, or subarachnoid hemorrhage, meningitis, nonconvulsive seizure, postictal state, or metabolic disorder.

Related questions.

1.What are the symptoms and how do you diagnosis Acute Confusional Migraine?

ACMs are named by their most prominent symptom, confusion, which means that the sufferer is disoriented as what happened in the time just before the attack started and for a varying period of time afterward.  The child may be restless or listless and vague in answering questions.

A state of intense confusion commences suddenly and lasts longer than the headache. The average episode is approximately five hours, but an event can be as short as 30 minutes or as long as 24 hours.

ACM symptoms are:

headache

memory loss

anxiety

agitation

blurred vision

dizziness

speech impairment

disorientation, or a loss of a sense of place and time

The patient is not allowed to have focal abnormalities on neurologic exam such as pupillary or eye movement disorder, a stiff neck, abnormal deep tendon reflexes or Babinski sign, focal weakness such as mono or hemiparesis or sensory loss.

After the episode patients fall into deep sleep and then recover.  Something like recovery from a migraine may involve deep sleep and then arouse to being headache free.  After recovery patients are amnestic for what happened during the event and the symptoms of memory affectation fade away.

The most common risk factor for ACM is to have a personal or family history of migraine.

To get up to date on Migraine please read my website article on doctormigraine.com on “What is Migraine.” Click here to read.

Read my Mini Book on Migraine Here.

2.What Causes ACM?

The cause of ACM is not certain, and more time and analysis of neurologic cases is necessary.  Forty percent of patients develop their attack after a mild bump on the head, which is usually a mild non-concussive event.  It isn’t clear what causes an ACM, and research about what might trigger this is ongoing. More ACM cases are being studied with neuroimaging.

ICHD-3 states that migraine triggers should be quick, now, onset within 24-hour features fasting or fever, while longer acting features such as stress should be called “Aggravating Factors.”

ACMs may have triggers or aggravating factors just like migraine does.  Migraine triggers or aggravating factors are:

Stress/nervous excitement

Freedom from stress-the letdown/weekend/holiday headache

Menstruation with fluctuating estrogen level

Oversleeping/undersleeping/insomnia/irregular sleep patterns

Hypoglycemia related to fasting

Barometric pressure change

Fever

Heat/sun/workout headache

Flashing/flickering/fluorescent/bright light

Prolonged overexertion

Motion sickness

Odors/fragrances/cigarette smoke

Head injury/concussion/post-concussion

Loud noises

Certain foods such as wine, chocolate, hot dogs

The exact pathophysiologic cause of ACM  is unclear but the common hypothesis or mechanism is that the confusional state is a complex aura phenomenon involving a cortical spreading wave of depression which occurs not only in the occipital, but also the temporal, parietal and frontal cortex, causing transient hypoperfusion and dysfunction of these brain areas.

This hypothesis is consonant with the as yet uncertain understanding of the but similar phenomenon of transient global amnesia which also links to migraine.

 3.What is the differential diagnosis of Acute Confusional Migraine?

A physician confronted with an acutely ill and confused child should rule out certain conditions with the neurologic exam, blood count and chemistry evaluation, urine and serum drug screen, CAT or MRI scan, and Electroencephalogram (EEG).  Patients with fever and a stiff neck should have spinal fluid examination.

All tests should be normal except the EEG which may sometimes show slow waves of the delta frequency diffusely or bioccipitally. With later clearing of sensorium in the child the EEG reverts to normal.

Consideration should be given to epilepsy, cerebral ischemia or  hemorrhage causing a stroke, neoplasm, intoxication, and encephalitis.

For patients with Acute Confusional Migraine all of the historical, exam and lab data should be normal except for mild head injury in 40 %.

4.How does migraine link to amnesia?

The next cases for question 4 come from my textbook, Transient Global Amnesia, listed on Amazon as a print and eBook.  Go to www.doctormigraine.com/shop/shopbooks/ find TGA.

Definition of Amnesia

 Benson,[i] writing about Amnesia in the Southern Medical Journal in 1978 stated that:

“Amnesia is a common clinical problem characterized by four features:  (1) normal immediate recall, (2) impaired ability to learn, (3) relatively spared ability to retrieve previously learned material, and (4) preserved cognitive and personality characteristics.”

Cases of Migraine and Amnesia

These are not cases of transient global amnesia but cases which detail the early literature regarding migraine and amnesia.  Liveing,[ii] neurology’s supreme cataloger and savant regarding all things to do with migraine wrote in 1873:

We have next to consider the disturbance of the higher cerebral faculties which sometimes attends the megrim paroxysm; this may be regarded for the most part as either intellectual or emotional.  The former is represented in some instances by loss or impairment of memory, and in others by confused, incoherent, or tumultuous ideation, very rarely by hallucination; the later by general depression, or vague subjective feelings of anxiety and dread.…

At this period (i.e., following the affections of sight and touch) her intellect becomes confused, and her memory at the same time, for about half an hour, so much impaired that she cannot even remember the name of any medicine she has just taken…

… as the visual phenomenon passed off his memory usually fail so much that for a time, he was mentally incapacitated, and whatever he read or did during that period left no impression….”

 Liveing did not describe the typical benign TGA episode but he wrote an encyclopedic monograph[iii] in which he recorded the mental symptoms that his patients had experienced during attacks. Sixteen out of 67 of Liveing’s patients had confusion, trouble with memory, or a disturbance of consciousness.  Nine of the 67 patients had the onset of migraine before age 20, and the youngest was at age 9.  After Liveing confusion as part of a migraine attack was rare in the neurologic literature.

Flatau[iv] writing in Handbuch Der Neurologie in 1914 on “Die Migrane und ihre Abarten” confronted the problem of migraine and mental symptoms.  Flatau called the problem "Dammerzustande" and proposed that the term migraine equivalent not be used unless:

The psychosis occurs in a person who also suffers from unquestioned migraine attacks; when the cessation of the hemicrania and the beginning of the psychosis approximately correspond in point of time; and when the form of the psychosis is the form most frequently encountered in migraine, i.e., confusional migraine.

Moersch[v] writing in 1924 in the American Journal of Psychiatry on “Psychic manifestations in Migraine” said that “During the clouding of consciousness, amnesia frequently occurs” and reported two patients with amnesia during migraine attacks.  Moersch’s review of the literature included:

 Hall[vi] in 1840 noted the relationship of sick headaches to psychic disturbances, such as stupor, delirium and unconsciousness.  Liveing,[vii] in his excellent review of the subject in 1873, tabulated 67 cases of migraine; in 21 of these “emotional and intellectual disorder,” such as confusion, impaired memory, depression, ill humor, drowsiness, terror, and so forth, were noted.  Mingazzini[viii] coined the term “dysphrenia hemicrania transitoria” to describe these psychic alterations, and classified them as abortive, transitory, or protracted.  Flatau[ix] considers that migraine psychoses are an entity, and not to be confused with epileptic equivalents.  In his study he found that the confusional states (Dammerzustande) are the most commonly associated mental changes.

One of Moersch’s cases with memory loss follows:

 Case 1—A man, aged 42 years, had had periodic sick headaches associated with scotomas, nausea and vomiting, since the age of four.  There was no history of migraine in the family.  In July 1918, he awakened a friend by talking in a natural voice of happenings of the day before.  He was lying limp in bed and could not be aroused, but had no convulsions.  After about 20 minutes he regained consciousness, was extremely nauseated, and for two or three days had a severe bitemporal headache.  In June, 1920, a similar attack occurred during the day, in which he suddenly, while walking, became confused in mind.  This state lasted for about ten minutes, and was followed by nausea, headache and vomiting for the greater part of the day.  In July, and again in August of the same year, he had spells of a similar character with a sudden lapse of memory, lasting for from 5 to 20 minutes, and followed by nausea, headache, and vomiting.  From that time up to the present, he has had several attacks in which he has even fallen, but has never had convulsions.  The attacks are always followed by nausea and headache, and usually by vomiting.  The general and neurologic examinations were negative.

Moersch commented:

When one realizes the vagaries of migraine, there seems every reason to believe that these interparoxysmal mental changes are an index of the innate constitutional make-up.  It is possible that many of the peculiarities which are ascribed to certain persons, such as occasional vague visual phenomena, mild recurring headaches and apathy, periodic mental dullness or other periodic mental fluctuations, are larvated forms of migraine.  It is also true that the headache in a migraine attack may be replaced entirely by a visual aura which, in turn, is followed by a psychic disturbance.

 Moersch’s cases were not the typical attack described by Bender, however, with anxiety, retrograde amnesia, and repetitive questioning.

Nielsen[x] writing in the American Journal of Psychiatry in1930 on “Migraine Equivalent” commented that “Psychic disturbances entirely replacing the usual symptoms of an attack of migraine have led to a great deal of discussion and some controversy during the last three decades.” In this article Nielsen reported a single case:

The patient is a physician, aged 37, who comes with no complaint except episodes of mental disturbance.  These do not incapacitate him; but he has worried for years about their possible significance, because genius and dementia praecox occur in the family of a paternal half uncle; and he has consequently feared for his own mental state.  Aside from the above facts he knows of no nervous or mental disturbances or of migraine in the family.

The attacks of mental disturbance may be described as follows:  He feels a mild emotional depression come on.  Things in general seem serious.  Then a feeling of strangeness supervenes and this is followed by a peculiar confusion.  During this he is perfectly oriented yet cannot give an orderly account of anything.  He is in possession of a multitude of facts concerning medicine and his environment, but there are large defects in his memory and hence organization of his knowledge is lacking.  Actually the defects are so large that it seems to him as though only small groups of facts make their unbidden appearance in his consciousness.  This isolation of facts and events, he says, is the outstanding difficulty in the episode.  There is no association of any kind between these groups of facts.  Further, he remembers nothing during an attack for more than half a minute.  He says he feels as though he sees events through a long tube or under the high power of a microscope and is unable to establish the relations between the various fields observed.  He can move the tube to another field, but then has no recollection of the one just observed.  This soon leads to confusion.

Practically, this state has the following effect.  He cannot recall events, lodge pass-words, formulas, dates, names, appointments, or promises at will.  They may all come to him but he cannot command them.  It is difficult for him to carry on a conversation because he cannot recall at any moment the last statement.  By the time he receives a reply to a question he does not know what he has asked.  Consequently he cannot deal with people, cannot take a history from a patient, cannot dictate.  He repeats questions and appears to others very absent-minded.  He feels as though he were in unfamiliar surroundings and everything seems unreal.  The unreality is the most distressing, feature of the whole episode, he states.  Fortunately the disturbance lasts only from three to six hours and the episodes appear only about once in every 6 to 12 months.  After the episode he has a perfect recollection of the events and can recall all his confusion and embarrassment.

After studying medicine he became more observant and noticed that a severe nervous or mental strain frequently preceded the attack.  He was questioned for symptoms of migraine but persistently denied any tendency toward migraine until fractional attacks were discussed and fortification spectra were shown to him.  It was then revealed that he suffered from attacks which he had never understood, referable only to the eyes.  These attacks also followed unusual strain but were never associated with the mental symptoms described above.  They began as blind spots with concentric rings running in the upper right quadrants of the fields of vision.  Soon they would spread to become a quadrant amblyopia or a right homonymous hemianopsia.  At times both upper halves of the fields of vision were involved.  He had great difficulty driving a car during an attack and could not read ordinary print because of inability to follow a line.  These disturbances were always sooner or later accompanied by typical fortification spectra.  These attacks were never accompanied by nausea, headache, pain, dizziness, or weakness, but were associated with a very mild confusion.  The invariably lasted only 15 minutes to one hour and were considerably more frequent than the attacks of confusion described in the foregoing. 

 Other reports on Acute Confusional Migraine and Transient Global Amnesia.

Sheth, RD, Riggs JE, Bodensteiner JB wrote in Pediatr Neurol in 1995 Feb;12(2):129-31 at the

Department of Neurology, West Virginia University School of Medicine; Morgantown, USA on Acute confusional migraine: variant of transient global amnesia.  The abstract of this article follows:

Acute confusional migraine in children and transient global amnesia in adults share a number of similar clinical manifestations. Acute confusional migraine in 6 children (mean age: 11.7 years; range: 7.5-17 years) was characterized by transient episodes of amnesia and acute confusion lasting 1-12 hours. Episodes were preceded by headache and vomiting in 4 patients. In 2 patients acute confusional migraine was the initial symptom. A history of preceding trivial head injury was reported in 3 patients and migraine in 4. Urine and serum drug screens were negative. Cerebral imaging studies and interictal electroencephalograms were normal. Ictal electroencephalograms in 3 patients revealed diffuse or bioccipital delta wave slowing. Recurrent episodes of acute confusional migraine occurred in 2 children during 1-3 years of follow-up. The clinical manifestations of acute confusional migraine in this series of children are similar to those reported in transient global amnesia. The similarity of the clinical manifestations of acute confusional migraine in children and transient global amnesia in adults suggests that these disorders may share a common pathophysiology.

Jensen, T.S. wrote in Dev Med Child Neurol Oct;22(5):654-8 on Transient global amnesia in childhood.  The abstract of this article follows:

Transient global amnesia, a brief disorder of recent memory affecting middle-aged and elderly patients, is probably caused by transient ischaemia of the hippocampal regions and other parts of the limbic system related to memory functions. A 13-year-old boy with a single episode of transient global amnesia and a three-year history of recurrent headache is described. It is suggested that some acute confusional states encountered in children with migraine may represent obscured instances of transient global amnesia, and that a brief vasoconstriction of the arteries supplying hippocampal structures is probably responsible for both conditions.

 Schipper S1, Riederer F, Sándor PS, Gantenbein AR wrote in Expert Rev Neurother. 2012 Mar;12(3):307-14. doi: 10.1586/ern.12.4 on Acute confusional migraine: our knowledge to date.  Their abstract follows:

 Acute confusional migraine (ACM) is a rare migraine variant, affecting children and adolescents, as well as adults. Between 0.45 and 7.8% of children with migraine present with ACM, but the disorder may well be underdiagnosed. ACM is an exclusion diagnosis and some dangerous causes of confusion (e.g., epilepsy, ischemia, hemorrhagia, neoplasm, intoxication and encephalitis) should be ruled out. The confusional state often manifests with a wide diversity of cortical dysfunctions, such as speech difficulties, increased alertness, agitation and amnesia. Exact history taking, clinical examination, and laboratory, radiological and electroencephalographical findings lead the practitioner towards the diagnosis. Approximately half of the cases may be triggered by mild head trauma. Transient global amnesia is an important differential diagnosis, possibly caused by similar pathophysiological mechanisms. The exact pathomechanism remains unclear, with the common hypothesis comprising of the confusional state as a complex aura phenomenon, in which the cortical spreading depression wave reaches not only the occipital, but also the temporal, parietal and frontal cortex, as well as the brainstem and the hippocampi, leading to transient hypoperfusion and dysfunction of these brain areas.

Pacheya I, Ivanov, I wrote in Int J Clin Pract 2013 Mar;67(3):250-6. doi: 10.1111/ijcp.12094 on

Acute confusional migraine: is it a distinct form of migraine?  The abstract of their article follows:

The International Classification of Headache Disorders (ICHD-II) - 2004 recognizes many migraine variants (different from migraine without aura and migraine with typical aura), but acute confusional migraine (ACM) remains unclassified and most clinicians are not well acquainted with it.

AIM:

The aim of this study was to illustrate ACM in the neuropaediatric practice, to discuss its place in the ICHD-II and to propose diagnostic criteria.

PATIENTS AND METHODS:

A total of 2509 files of newly diagnosed patients, aged 0-18 years, treated as in- and outpatients in the Neuropaediatric Ward at the Plovdiv Medical University Hospital between 2002 and 2006 were screened retrospectively. Their diagnosis was based on detailed medical history, physical and neurological examination, additional functional, imaging and laboratory investigations. Migraine and migraine variants were diagnosed according to ICHD-II, but specific forms (e.g. ACM and Alice in wonderland syndrome) were also included.

RESULTS:

One hundred and eleven patients met the diagnostic criteria for migraine. Migraine variants comprised 24.3% of all migraine cases. In particular, ACM represented 11.1% of migraine variants or 2.7% of migraine and 0.12% of all paediatric neurological diseases. Here, we report three cases of ACM with analysis of the typical clinical and EEG features, review the literature and propose diagnostic criteria.

CONCLUSION:

ACM may present as either the only manifestation of a migraine attack or in the context of other migraine forms. ACM should have its own distinct place in the ICHD-II, may be as a subtype of migraine with complex aura.

Farooqui A.M., Padilla J.M. Monteith T.S. wrote in Brain Sci 2018 Feb 7;8(2) on Acute Confusional Migraine: Distinct Clinical Entity or Spectrum of Migraine Biology.  Their abstract follows:

The goal of this review is to explore the literature reports of acute confusional migraine (ACM) including patient characteristics, migraine symptomatology, and proposed diagnostic criteria. A literature review was conducted using PubMed, Scopus and Web of Science using the terms "confusional migraine" and "confusional state in migraine". All the relevant articles from 1970 to 2016 were included. A total of 120 patients were found in the literature. Most of the cases were seen in the pediatric population with a slight male predominance. Personal or family history of migraine was common. Most patients had a headache prior to the confusional state. In addition to confusion and agitation, some developed visual (32.5%) and/or sensory symptoms (19%) and/or speech problems (39%) either prior to or during the confusional state. Data on treatment outcomes is lacking. Patients with most common forms of migraine report attention and cognitive disturbances but awareness remains intact as opposed to patients with ACM. ACM is a distinct entity and should be included as part of the appendix of International Classification of Headache Disoders-3 beta version (ICHD-3β) criteria. Prospective studies are needed to further study this disorder and its association with other migraine forms.

Rota E1, Morelli N, Immovilli P, Mitri PD, Magnifico F, Terlizzi E, Mazza L, Sala B, Biasucci G, Guidetti D. wrote in Case Rep Neurol. 2012 Sep;4(3):240-3 on 'Possessed': acute confusional migraine in an adolescent, prevented by topiramate.  Their abstract follows:

Acute confusional migraine (ACM) is recognized as a rare, but highly disabling migraine equivalent, mostly reported in children and adolescents. Herein we describe the case of a 12-year-old girl admitted to hospital for an acute confusional state and severe psychomotor agitation, associated with a pulsating headache and nausea, which turned out to be a manifestation of ACM. The girl was discharged on topiramate prophylaxis, titrated up to 75 mg/die; no recurrence of confusional and/or headache episodes has been reported over the last 14 months to date. Due to the rarity of this clinical entity, only anecdotal reports about acute and prophylactic treatment of ACM are available in the literature. The case reported herein suggests that topiramate seems to be effective in ACM prophylaxis, although a longer observation period in our patient and more cases are needed to confirm any long-term clinical benefit.

 5.Who is at risk of getting ACM?

Having a family history of migraine is the most prevalent risk factor for ACM. Eighty percent of persons who have migraine will have someone in their family with migraine.  Remember that migraine is the most common medical condition of all in women, posting a frequency of 25%. Half or 50% of ACMs occur in persons who have had one or more episodes of migraine.

6.How Is an ACM Treated?

The attacks are self-limited, lasting usually up to 6 or 24 hours and then improved after sleep. Patients are usually assessed by emergency room doctors or pediatric neurologists in the hospital or the clinic.  Since migraine is a genetic problem and the genome for migraine has been figured out, then persons are born with a tendency to get migraine and they’re going to die with that tendency to have migraine unless a means to reverse the genetic nature of migraine is developed.  This is not available currently.

The headache part of ACM can be treated by medication used for treatment of migraine in general.  This includes acute therapy drugs for headache:

Over the counter painkillers like Excedrin, Advil, Tylenol, or Aleve.

Any of the acute therapy triptans such as sumatriptan, rizatriptan, eletriptan, zolmitriptan, or almotriptan may be used.

Events of ACM may be prevented by daily use of common preventive drug for migraine such as, topiramate, valproic acid, amitriptyline, or propranolol.  The new CGRP antibodies may be tried but there is no data on using them for treatment now.

Katis[xvi] summarized treatment options with the following statement that “anti-migraine medications like sumatriptan, dihydroergotamine), metoclopramide, and prochlorperazine may be useful, as may prophylactic agents such as beta-blockers and calcium-channel blockers, but none of these agents have been systemically studied…”

Literature review of migraine and transient global amnesia.

Liveing wrote in 1873:[i]

We have next to consider the disturbance of the higher cerebral faculties which sometimes attends the megrim paroxysm; this may be regarded for the most part as either intellectual or emotional.  The former is represented in some instances by loss or impairment of memory, and in others by confused, incoherent, or tumultuous ideation, very rarely by hallucination; the later by general depression, or vague subjective feelings of anxiety and dread.

At this period (i.e., following the affections of sight and touch) her intellect becomes confused, and her memory at the same time, for about half an hour, so much impaired that she cannot even remember the name of any medicine she has just taken…

… as the visual phenomenon passed off his memory usually fail so much that for a time, he was mentally incapacitated and whatever he read or did during that period left no impression…”

Living wrote an encyclopedic monograph[ii] in which he recorded the mental symptoms that his patients had experienced during attacks.  Sixteen out of 67 of his patients had confusion, trouble with memory, or a disturbance of consciousness.  Nine of the 67 patients had the onset of migraine before age 20, and the youngest was at age 9.

After Liveing confusion as part of a migraine attack was rare in the neurologic literature.  Whitty in 1953[iii] writing about “Familial hemiplegic migraine” described a 52-year-old woman who had prolonged confusion for a week after a migraine attack.  Selby and Lance in1960[iv] wrote about mental confusion as a feature of their migraine in 14 of 396 patients.  Wolff[v] in 1963 reported a 20-year-old female with migraine who developed mental clouding with hemiplegia and aphasia.

Gascon and Barlow[vi] writing in 1970 in Pediatrics on "Juvenile Migraine, Presenting as an Acute Confusional State" said the following regarding childhood migraine:

Migraine in childhood differs from that an adult life in several ways.  Attacks are generally shorter, although occasionally a bout is prolonged and may last several days.  Prodromal symptoms, such as visual phenomena, are less marked, and gastrointestinal upset is more intense.  Often gastrointestinal stress is a sole manifestation, as in the syndrome of "cyclic vomiting of childhood," which we frequently find to represent a form of migraine ontogenetically preceding more recognizable attacks with headache.

Gascon and Barlow stated that the purpose of their paper was, "to call attention to a clinical form of the migraine syndrome where the most prominent manifestation of the attack was impairment of the sensorium resulting in an acute confusional state."  They summarized the clinical features of their 4 patients by stating:

Our patients all showed defects of sensorium, impaired awareness of their environment, and slow response to external stimuli such as pinprick or questions from examiners.  One boy, the youngest in the group at age 8, manifested hyperactivity, restlessness, and combativeness, accompanied by obscene language.  When memory was specifically testable, there was a defect in recent memory, with partial retrograde amnesia for the events preceding the attack.

Emery wrote in 1977[vii] in Pediatrics about "Acute Confusional State in Children With Migraine."  He pointed out that:

a wide variety of paroxysmal visual, sensory, and motor disturbances with or without headache is included in the migraine syndrome, but disturbances of consciousness and mental functioning as part of the migraine syndrome in children are not well recognized.

Emery presented 4 patients aged 8-13 and 2 of them had mild preceding trauma.  Emery’s Case 1 follows:

An 8-year-old girl fell off her sled and rolled down a hill.  After she walked home approximately 400 m, her parents observed confused, fearful, agitated, and combative behavior.  Because this abnormal behavior persisted in the emergency room of the local hospital, she was transferred to the Medical Center Hospital of Vermont.

Her first EEG performed 7 hours after onset of symptoms and when she was still confused and agitated, showed a high voltage polymorphic delta activity more dominant over the left side.  This child remained agitated and confused for approximately 9 hours when she fell asleep and after she awoke 4-5 hours later, she was alert and had a normal neurologic exam.  She was followed for 3 years and had intermittent, severe headaches.

Regarding Case 2 Emery described:

A 5 year-old boy, playing outside with his brother, slipped on the ice and bumped his forehead, without loss of consciousness.  He came into the house, ate lunch, and complained of a headache.  After napping for one hour, he acted confused and did not recognize his mother.  His speech was garbled.  He was not blind.  When examined in the emergency room of the local hospital, he is described as appearing pale and sweaty, with slurred speech and "talking nonsense."  He vomited several times.  He had a past history of mild, infrequent, and nonspecific headaches.  His mother had a history of bifrontal, throbbing headaches associated with nausea.

When the child was examined at the Medical Center Hospital of Vermont approximately five hours after the onset of the confused state, he would give his name on request, but the remainder of his speech was either unintelligible or incoherent.  When re-examined one hour later he was coherent and oriented, but lethargic.  He was amnesic for the 5 hour period between his nap and admission to the hospital.

The boy in Case 2 had an EEG performed 12 hours after the onset of his confusional state which showed a bioccipital high-voltage delta wave more prominent over the right hemisphere.  A third EEG 3 weeks later was normal.  During his 4 day hospitalization his exam was normal although he complained of intermittent, unilateral, alternating headache and abdominal pain.

Menken wrote in 1978[viii] in Clinical Pediatrics on "Transitory Confusion After Minor Head Injury," in which he described two boys, ages 16 and 15 who had severe confusion after minor head trauma.  Menken thought that the:

antecedent head trauma seemed so trivial that it was initially ignored in the differential diagnosis which considered toxic and metabolic encephalopathies, encephalitis, ictal or postictal confusional states, and drug intoxication.

He also described a common problem in pediatric neurology:

Neurologists and neurosurgeons with pediatric experience are familiar with the not infrequent syndrome of irritability, vomiting, and variable somnolence following minor head trauma.  These children are difficult to examine, resisting fundoscopy for example, and drift off to sleep when unattended.  The basis for the syndrome is unknown since it is fully reversible, and no pathologic material has been studied.

Ehyai and Fenichel in 1978[ix] wrote in Child Neurology on "The Natural History of Acute Confusional Migraine.”  They described 4 cases in children aged 9 to 14 years old.  They felt that in these patients "typical migraine headaches always developed eventually."  They noted that when the patient was first seen in a confused state and there was no history of migraine it was difficult to make a diagnosis so that a family history of migraine became an important clue.  They reported on the “natural history” of the problem by following Case 1 for 21 months, Case 2 for 18 months, Case 3 for 5 years, and Case 4 for 26 months.

Ehyai and Fenichel’s Case 5 follows:

A 14-year-old girl suddenly became disoriented while at school.  She was agitated and walked purposely in the hall, complaining of blurred vision.  Her speech was rapid but incomprehensible.  The agitated confusion lasted for a few hours; then she fell asleep and awoke the next morning with amnesia for the event.  A second identical episode occurred two days later.

She was examined at our hospital one week later and found to be normal.  Both the patient and her mother had had typical migraine for several years.  The patient's most recent migraine occurred two weeks prior to the first confusional episode.  She was treated with sublingually administered ergotamine, which was of some benefit.  During 26 months of observation, no further confusional states were recorded.

Ferrera and Reicho[x] writing in the American Journal of Emergency Medicine in 1996 on “Acute confusional migraine and trauma-triggered migraine” described 2 cases of children with histories of “confusion and agitation.”  One of their cases had multiple episodes after mild head trauma.  They noted that “transient blindness and hemiplegia may accompany the confusional state.”

Sakas, et al,[xi] wrote a paper in Neurosurgery in 1997 the purpose of which was to “explain the pathophysiology of the neurological deterioration that occurs after trivial head injuries in children that is not caused by focal structural brain damage.”  They noted that the symptoms and/or signs included “headache, confusion, drowsiness, vomiting, hemiparesis, cortical blindness, and seizures.”  They noted that the assumption in this situation had been that underlying cerebral edema was responsible for these phenomena, but this had been proven incorrect by cerebral imaging studies.  They proposed that:

children who are susceptible to such neurological attacks have an unstable ‘trigeminovascular reflex’ which is activated by craniofacial trauma…head trauma activates trigeminal nerve endings in the face, scalp, dura, or cortex, and via a reflex, causes intracranial vasodilation and cerebral hyperemia.

 Soriani, et al,[xii] writing in 2000 in Archives of Pediatric and Adolescent Medicine on “Confusional Migraine Precipitated by Mild Head Trauma” reported on 8 boys and 3 girls, aged 6-14 years who presented after mild head trauma with confusion.  In addition to confusion their patients also experienced agitation (5), visual disturbances (3), bilateral mydriasis (3), dysarthria (1), somnolence (6), vomiting (7), and headache (6).  None of their patients had seizures and the attacks lasted from 1 to 12 hours.  They stated that the presence of a confusional state after head trauma often moved the treating physician to perform more extensive diagnostic testing such as CAT or MRI scanning of the brain and possible hospital admission.  They stressed that:

However, the possibility that confusion is caused by a migraine attack triggered by minor head trauma must be considered.

Borusiak[xiii] wrote in 2001 in Klin Padiatr about an 11-year-old girl who presented with her first migrainous attack as a confusional state.  The diagnosis was made after the acute episode had subsided.  Katis writing in 2004[xiv] in Canadian Journal Emergency Medicine about acute confusional migraine (ACM) stated:

Children rarely present with auras, but often exhibit autonomic symptoms such as pallor, nausea, vomiting, and abdominal pain.  Discrete migraine equivalents or precursors have been observed from infancy to adolescence, in which headache is not prominent.

Katis stressed that confusional migraine is “a diagnosis of exclusion,” and the differential diagnoses should include “intracerebral injury, toxic ingestion, nonconvulsive seizure, post-ictal state, encephalitis, hypoglycemia, and metabolic derangement.”  He felt that if testing such as blood work, CT, and MRI scan are normal, and ACM seems likely that “treatment consists of simple analgesics and sleep.”  He stressed that symptoms “normally resolve within several hours, and almost universally resolve within 24 hours.”

Dr. David Rothner[xv] reported on 90 cases of acute confusional migraine at the annual scientific meeting of the American Headache Society in 2007.  In his patients confusion lasted from 10 minutes to 2 days, with the majority of patients remaining confused for 4 hours or less, but 25 (28%) were confused between 5 and 8 hours.  All the children were disoriented, 72 had amnesia, 63 had speech impairment, 49 had agitation, 49 had emesis, 36 had visual disturbances, and 33 had somnolence.  Seventy four children had a family history of migraine and 52 had a personal history of migraine.  More than a third of his patients had recurrent acute confusional migraine events.  Boys aged 5-12 years, followed by boys aged 13-17 years, were most commonly affected.  Head trauma which often was very mild was present in more than a third of his cases.  Dr. Rothner described:

… a 14 year-old girl who experienced an aura followed by a bifrontal headache and a 5-hour period of progressive disorientation, confusion, incontinence, bizarre behavior, and extreme combativeness.  Once the confusion passed, the patient had no recollection of these events.  Her parents recalled two prior episodes that were less severe and involved nausea and vomiting.

Toxicology screens in 76 of Rothner’s patients were negative as were spinal fluid examinations in 29.  CT or MRI in 63 patients was normal in 57 and showed unrelated abnormalities in 6.  Electroencephalograms in 55 patients were abnormal in 44 with most showing unilateral or bilateral slowing.

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Bibliography on Migraine and Confusional Migraine

[i] Livening, E.  Analytical table of cases.  On Megrim, Sick Headache, and Some Allied Disorders.  London:  J. and  A. Churchill, 1873.

[ii] Gascon G, Barlow C. Juvenile Migraine, Presenting As An Acute Confusional State.  Pediatrics.  1970;45 (4):628-635.

[iii] Whitty CWM.  Familial hemiplegic migraine.  J. Neurol. Neurosurg. Psychiat.  1953;16:172.

[iv] Selby G, and Lance JW.  Observations on 500 cases of migraine and Allied vascular headache.  J. Neurol. Neurosurg. Psychiat.  1960;23:23.

[v] Wolff  H.  Headache and Other Head Pain, ed.2 New York: Oxford University Press.  1963:342.

[vi] Gascon G, Barlow C. Juvenile Migraine, Presenting As An Acute Confusional State.  Pediatrics.  1970;45 (4):628-635.

[vii] Emery ES.  Acute Confusional State in Children With Migraine. Pediatrics.  1977; 60: 110-114.

[viii] Menken, M.  Transitory Confusion After Minor Head Injury.  Clinical Pediatrics.  1978;17:421-4.2.

[ix] Ehyai A, Fenichel GM. The Natural History of Acute Confusional Migraine.  Child Neurology.  1978;35:368-369.

[x] Ferrera PC, Reicho PR.  Acute confusional migraine and trauma-triggered migraine.  Am J Emerg Med.  1996;14(3):276-278.

[xi] Sakas DE, Whittaker KW, Whitwell HL, Singounas EG.  Syndromes of Posttraumatic Neurological.  Deterioration in Children with No Focal Lesions Revealed by Cerebral Imaging:  Evidence for a Trigeminovascular Pathophysiology.  Neurosurgery.  1997;41(3):661-667.

[xii] Soriana S, Cavaliere B, Faggioli R, Scarpa P, Borgna-Pignatti C.  Confusional migraine precipitated by mild head trauma.  Arch Pediatr Adolesc Med.   2000;154(1):90-91.

[xiii] Borusiak P.  First manifestation of migraine as acute confusional state:  “confusional migraine” and diagnostic problems.  Klin Padiatr.  2001;213(1):28-29.

[xiv] Katis PG.  Can J Emerg Med.  2004;6(6):451.

[xv] Rothner DA.  Cases Create Portrait of Confusional Migraine.  Clinical Neurology News.  March 2007:20.

[xvi] Katis PG.  Can J Emerg Med.  2004;6(6):451.

Bibliography from insert from TGA textbook

[1]    Benson DF.  Amnesia.  Southern Medical Journal.  1978;71(10):1221-1227,1231.

[1]   Liveing, E.  Analytical table of cases.  On Megrim, Sick Headache, and Some Allied Disorders.  London:  J. and  A. Churchill, 1873.

[1]   Gascon G, Barlow C. Juvenile Migraine, Presenting As An Confusional State.  Pediatrics.  1970;45(4):628-635.

[1]   Flatau E.  Die Migrane und ihre Abarten.  Handbuch Der Neurologie, Vol  V., Spezielle Neurologie IV, Lewandowsky M. (Julius Springer), Berlin 1914:342-411.

[1]   Moersch FP.  Psychic manifestations in migraine.  American  Journal of  Psychiatry.  1924;80:697-716.

[1]   Hall, M.  The neck as a medical region; hidden seizures; paroxysmal affections of the nervous system.  Lancet. 1849, ii, 66-69.

[1]   Liveing, E.  On Megrim, Sick Headache, and Some Allied Disorders.  London:  J. and A. Churchill,  1873,512 pp.

[1]   Mingazzini, G. Pacetti G.  Studio clinico sulle psicosi neuralgiche (in sensu lato).  Schmidts Jahrb. f. ges.  Med., 1902, cclxxii,254-255.

[1]   Flatau, E.  Die Migrane und ihre Abarten.  In:  Lewandowsky, M.:  Handbuch der Neurologie.  Berlin, Springer, 1914, v, pp.342-426.

[1]   Nielsen, JM.  Migraine Equivalent.  American Journal of Psychiatry.  1930;86(4):637-641.