CLASSIFICATION OF CEREBRAL PAROXYSMS IN DOGS AND

Transkrypt

CLASSIFICATION OF CEREBRAL PAROXYSMS IN DOGS AND
Acta Sci. Pol., Medicina Veterinaria 13 (1-4) 2014, 15-26
ISSN 1644–0676 (print) ISSN 2083–8670 (on-line)
CLASSIFICATION OF CEREBRAL PAROXYSMS
IN DOGS AND CATS, THEIR ETIOLOGY
AND DIAGNOSIS1
Nadija Ivanczenko1, Kateryna Grom1, Edyta Pasicka2,
Mykola Tsvilihovskiy1
National University of Life and Environmental Sciences of Ukraine, Kyiv,
Ukraine
2
Wrocław University of Environmental and Life Sciences, Wrocław, Poland
1
Abstract. The main goal of this review was to determine a proper patient assessment, understanding the principles of antiepileptic drug (AED) therapy, designing a strategy for
pharmacotherapy, and plans for emergency treatment. Literature review of the classification
of paroxysmal states in animals and their etiological factors and characteristics of manifestation were made. Information about the basic principles of diagnosis and staging of
primary as well as final diagnoses of cerebral paroxysms in animals was systematized. In
this article main principles of seizure management (paroxysmal disorder of cerebral function management) in dogs and cats are addressed. Particular attention is dedicated to canine
and feline epilepsy treatment.
Key words: classification, diagnosis, etiology, seizure
INTRODUCTION
The difficulty of diagnosis of animal central nervous system (CNS) diseases is that the
symptoms of its lesion are often nonspecific. Ascertainment of the final diagnosis is possible only by using special diagnostic methods that are not always available in clinical
practice. Recently, in Ukraine more attention is paid to veterinary neurology. And tendency of usage of “Western model” for diagnostics and treatment of animals is being formed.
© Copyright by Uniwersytet Przyrodniczy we Wrocławiu
Corresponding author – Adres do korespondencji: Edyta Pasicka, Division of Animal Anatomy,
Department of Biostructure and Animal Physiology, Faculty of Veterinary Medicine, Wrocław University of Environmental and Life Sciences, Kożuchowska 1/3, 51-631, Wrocław, Poland, e-mail:
[email protected]
16
N. Ivanczenko et al.
In our opinion the most confusion occurs in the diagnosis of seizures (Ss), including those
that are characterized by the development of cramping syndrome.
Ss are spontaneous stereotype abnormalities in animal behavior which are caused
by brain (B) damage (hemorrhage) and malfunction (abnormal electrical activity). The
term “convulsion” is used to indicate seizures with clonic generalized motor component.
Clinical manifestations of Ss depend on the location of injured neurons, their quantity and
peculiarities of passages of nervous impulses. In animals symptoms of Ss may include
changes in physical activity, sensitive areas, behavior or level of consciousness as well
as manifestation of the autonomic nervous system (ANS) (salivation, urination, defecation) [Oliver 1987]. Ss are always evidence of disturbance of function of the cerebrum
or diencephalon. Also temporal lobe and related structures of the limbic system are often
affected.
Physiological basis of paroxysmal disorders is excessive synchronous depolarization
of large groups of neurons that is the focus of paroxysmal activity. The activity of the
focus spreads to other parts of the brain, which leads to generalized cerebral dysrhythmia
(paroxysmal dysrhythmia), which by turn causes behavioral changes, known as Ss.
All processes that can influence the activity or structure of B, disrupt the homeostasis
of neurons and thus alter neural activity, can cause Ss [Lorenz and Kornegay 2004, Plat
and Olby 2004].
Classification of paroxysmal states
Etiologic factors that cause Ss, pursuant to anatomical classification, are conventionally
divided into extracranial and intracranial. Also Ss can be classified into primary or idiopathic and secondary or symptomatic. Ss may be generalized or partial, depending on the
part of the brain affected by abnormal electrical activity. Signs of partial seizures can be
separated into three categories: motor signs, autonomic signs, and paroxysms or behavioral signs [Berendt et al. 2004].
Extracranial attacks include those which are caused by generalized metabolic disturbances (metabolism of glucose and oxygen, electrolyte disorders – hypo/hypercalcemia,
hipo-/hipernatremia, hypomagnesemia, hypovitaminosises, disorders of neurotransmitters function), intoxications, diseases of the cardiovascular and respiratory systems, pathology of liver and kidneys.
Intracranial attacks are those that are caused by congenital or acquired brain injuries
(trauma, encephalitis, tumors, hydrocephalus, degenerative diseases, edema of B) and
idiopathies.
Generalized paroxysms (Table 1) [Oliver 1978] result from pathological processes
that usually cover brain, cerebellum, thalamus and midbrain reticular formation. It is
called primary generalized epilepsy if the cause of the Ss cannot be ascertained; the secondary generalized epilepsy (symptomatic epilepsy) – if any organic cause can be found
[Gastant 1969]. Primary generalized epilepsy includes idiopathic generalized epilepsy,
essential epilepsy, true epilepsy, genetic epilepsy and centrencephalic epilepsy [Holliday
1980].
Idiopathic epilepsy is a term used to denote the state of an organism which is characterized by recurrent neurological attacks for which it is not possible to find intra- or
extracranial causes. The brain structure of these animals is within the anatomical norm,
deviations are observed only in its functioning.
Acta Sci. Pol.
17
Classification of cerebral paroxysms...
Table 1. Classification of seizures: clinical signs
Tabela 1. Klasyfikacja ataków padaczkowych: oznaki kliniczne
Clinical manifestation
Manifestacja kliniczna
Etiology
Etiologia
Anatomic location
Lokalizacja anatomiczna
Generalized seizures, bilateral symmetric seizures, or seizures without local onset
napady uogólnione, napady dwustronne symetryczne lub napady bez lokalnego początku
Primary generalized, tonic-clonic
(grand mal, major motor)
Podstawowe uogólnione,
toniczno-kloniczne
(duże, konwulsywne)
1. Genetic predispositions
1. Predyspozycje genetyczne
2. Diffuse/multiple organic
lesions
2. Rozległe/liczne zmiany
organiczne
3. Toxins/metabolic disorders
3. Toksyny/zaburzenia
metaboliczne
1. Unlocalized/multilocal
1. Niezlokalizowane/multilokalne
2. Diencephalic
2. Międzymózgowe
Absences with/without motor
phenomena (petit mal) rare or
Usually genetic predisposition
rarely recognized in animals
(in humans)
Napady nieświadomości
Zazwyczaj predyspozycje
z/bez zjawisk konwulsywnych
genetyczne
(mały napad) rzadkie lub rzadko
(u ludzi)
rozpoznawane u zwierząt
Partial seisures or seizures beginning localy
Napady częściowe lub napady zaczynające się miejscowo
Partial motor
Acquired organic lesion of brain
(can be generalized to
Nabyte organiczne uszkodzenie
tonic-clonic seisures); signs
mózgu
depend on site of discharge
Sub/focal sub/cortical
Częściowo ruchowe
Podogniskowa/
(można uogólnić do
podkorowa
napadów toniczno-klonicznych);
objawy zależą od miejsca wyładowania
Psychomotor (can develop
to complex
Limbic system (hippocampus, tempobehavioral shifts, such
ral lobe, piriform lobe)
as running, fear, aggression)
Układ limbiczny (hipokamp, płat
Psychomotoryczne (mogą
skroniowy, płat gruszkowaty)
rozwinąć się do złożonych zmian
behawioralnych, takich jak
ucieczka, strach, agresja)
The most common generalized paroxysms in veterinary practice are generalized seizures (tonic-clonic seizure, grand mal/major motor convulsion). They are typical for idiopathic epilepsy in dogs. Generalized paroxysmal should be differentiated from syncope
and acute vestibular syndrome.
Other forms of generalized paroxysms are petit mal and myoclonic jerk.
Petit mal Ss (absence seizures, lapse attacks) are characterized by short duration (from
one to several seconds) with loss of consciousness’s connection with the environment or
complete loss of consciousness and muscle tone. Motor activity is not typical. This type
Medicina Veterinaria 13 (1-4) 2014
18
N. Ivanczenko et al.
of Ss is rare for animals. It is difficult to diagnose because of the symptoms’ similarity to
cataplexy, narcolepsy or episodic weakness.
Myoclonic jerks are generalized Ss, which are characterized by a strong spontaneous
jerk of most of the bodily muscles. They are also rare in veterinary practice.
Partial (focal) motor Ss generally indicate intracranial pathology and reflect the activity of focus of paroxysmal activity in the brain’s motor area. Partial Ss are also called
“cortical epilepsy”. Involuntary movements are restricted to one part of the body such
as face or limb. Partial Ss are always contracted and frequently spread, resulting in a
generalized convulsion. This type of Ss also includes Jacksonian epilepsy, but it is rare
for animals.
Partial Ss may also spread from non-motorized areas of B, for example from the visual cortex, parietal cortex, limbic system. In these cases, the manifestations of ANS are
dominate. Neurological symptoms include aggression, aimless running/moving forward,
howling/whining, blindness, hypersalivation, abnormal licking, bulimia, allotriophagy.
Such Ss are also called psychomotor, complex partial or behavioral ones and in English
literature – floor-licking seizures. In animals the possibility of development of psychomotor Ss with sensory component can be recognized [Lorenz and Kornegay 2004].
Pathological conditions that can cause Ss in dogs and cats
Neurological abnormalities in dogs and cats are often caused by pathology of development. They can be inherited or not, but they are not the primary generalized (genetic) epilepsy, as the structural changes in brain can be accurately determined. Besides,
it must be considered that there may be several congenital pathologies at the same time.
For such breads as German Shepherd, Beagle (Beagles are especially prone to develop
epilepsy), Belgian Sheepdog (Tervuren), dachshund, Horak’s laboratory dog, Irish Setter (assumed), German Spitz (Keeshond) genetic causes are typical; for Labrador Retriever, Golden Retriever, Irish Setter, Poodle (Miniature, Standard), St. Bernard – idiopatic causes; for Boston Terrier, Chihuahua, Miniature Pinscher, Toy Poodle, Pekingese,
Yorkshire Terrier – hydrocephalus; for Boston Terrier and Boxer – neoplasia; for Lhasa
Apso – lissencephaly; for English Setter, German shorthaired pointer – lipodystrophy; for
Cairn Terrier, West Highland White Terrier – globoid cell leukodystrophy; for Miniature
Schnauzer, Maltese, Yorkshire Terrier – portocaval shunt; for Miniature Schnauzer – hyperlipo-proteinemia; for Cocker Spaniel, Collie, Siberian Husky, Wire Fox Terrier – the
high incidence [Holliday 1980, Oliver 1980, Oliver 1987, Hall and Wallace 1996, Famula
and Oberbauer 2000, Lorenz and Kornegay 2004].
Hydrocephaly (congenital or acquired) causes an increase of intracranial pressure
(IP). Neurological symptoms can range from mild depression to severe convulsions.
Moreover, in cats and dogs there are cases of porencephaly and hydranencephaly.
Otocephalic syndrome which is transmitted hereditarily was described in beagles.
It is characterized by craniofacial anomalies and hydrocephalus of various degrees of
manifestation of the disease. Epileptoid nervous disorders occur in dogs which reach
sexual maturity.
Hereditary transmission of lissencephaly and pachygyria was registered in cats and
certain breeds of dogs. Lissencephaly includes behavioral, visual and convulsive disorders, and also leads to changes of mental status (oppression, agitation). Symptoms usually
appear within the first year of the animal’s life (Table 2) [Oliver 1980].
Acta Sci. Pol.
19
Classification of cerebral paroxysms...
Table 2. Causes of paroxysmal states depending on the dog’s age
Tabela 2. Przyczyny stanów napadowych w zależności od wieku psa
Class of disease
Klasa schorzenia
Cause
Przyczyna
< 1 year
< 1. roku
Degenerative
Zwyrodnieniowe
Developmental
Rozwojowe
Intoxication
Zatrucie
Infections
Zakażenia
Metabolic
Metaboliczne
Nutritional
Odżywcze
Parasitic
Pasożytnicze
Traumatic
Urazowe
Storage diseases
Choroby spichrzeniowe
Hydrocephalus
Wodogłowie
Lead, organophosphates, chlorinated hydrocarbons
Ołów, fosforany organiczne, węglowodory chlorowane
Canine distemper, infectious canine hepatitis, feline viral rhinotracheitis,
other infectious diseases
Nosówka psia, choroba Rubartha, wirusowe zapalenie nosa i tchawicy
kotów, inne choroby zakaźne
Hypoglycemia (transient), fermentopathy, portocaval shunt, hepatic encephalopathy
Hipoglikemia (przejściowa), fermentopatia, zespolenie wrotno-systemowe
zastawki, encefalopatia wątrobowa
Hypovitaminosis, electrolyte imbalances, hypertonic dehydration of the
brain cells
Hipowitaminoza, zaburzenia równowagi elektrolitowej, odwodnienie
hipertoniczne komórek mózgu
Direct invasion of the CNS
Bezpośrednia inwazja OUN
Brain concussion/trauma, penetrating wounds
Stłuczenie mózgu/trauma, rany penetrujące
1–3 years
1–3 lata
Usually the first paroxysm in dogs occurs at the age of 1–4 years
Zazwyczaj pierwszy paroksyzm u psów pojawia się w wieku 1–4 lat
Primary generalized epilepsy (8 weeks – 6 months – 5 years old);
Genetic
other as above
Genetyczne
Pierwotnie uogólniona padaczka (wiek 8 tygodni – 6 miesięcy – 5 lat);
pozostałe jak wyżej
> 4 years
> 4 lata
Hypoglycemia (secondary, because of β-cells neoplasms), hypocalcemia
Matabolic
(hypoparathyroidism), hepatic encephalopathy (cirrhosis)
Mataboliczne
Hipoglikemia (wtórna, z powodu neoplazmów komórek β), hipokalcemia
(niedoczynność przytarczyc), encefalopatia wątrobowa (marskość)
Neoplastic
Primary, secondary (metastatic)
Nowotworowe
Pierwotne, wtórne (przerzutowe)
Vascular
Cardiovascular system (arrhythmia, thromboembolism)
Naczyniowe
Układ sercowo-naczyniowy (arytmia, choroba zakrzepowo-zatorowa żylna)
Medicina Veterinaria 13 (1-4) 2014
20
N. Ivanczenko et al.
Congenital enlargament of the foramen magnum was described in toy breeds of dogs.
Clinical symptoms occur in dogs at the age of 2–6 months. Symptoms range from cervical pain to Ss.
Ss can be caused by neurodegenerative diseases, which are associated with the deposition of metabolic products in the nervous tissue (NT). For example, among hereditary
lipidosis, which affect small animals, GM2 gangliosidoses and neural glycoproteinosis
(Lafora disease or myoclonic progressive familial epilepsy) were found.
Ss may also be caused by deficiencies of B-group vitamins (thiamine, riboflavin, niacin, pantothenic acid, biotin).
In dogs thiamine deficiency causes paraparesis, resulting later in tetraparesis, convulsions and coma. In cats Ss are characterized by ventroflexion of the neck, kyphosis,
ataxia, hyperesthesia, behavioral changes, mydriasis and coma.
Lack of riboflavin in the dog organism is recognized clinically by local seizures, ataxia and convulsions.
Deficiency of niacin and pantothenic acid cause such neurological symptoms as weakness, convulsions, coma which results in death.
Hypocalcemia сan lead to attacks such as grand mal or ventroflexion of the neck. Seizures are characterized by discontinuity and only temporary efficacy of anticonvulsants.
There is evidence that respiratory alkalosis may cause seisures in susceptible dogs.
Neurological symptoms of hypoglycemia include oppression, paresis of hind limbs,
seizures, grand mal.
Uremia affects both CNS and peripheral (PNS) nervous systems, causing behavioral
abnormalities, uncoordinated movements, tetany and convulsions.
Hepatic encephalopathy is manifested by depression and stupor, and can cause blindness, behavioral abnormalities, aggression, ventroflexion of the neck, motor dysfunction,
as well as grand mal. The development of tetraplegia and miosis is also possible.
Hypothermia can lead to Ss, coma and death.
Neurological symptoms of hyperthermia can vary from slight depression to stupor,
convulsions and coma.
Deficit of oxygen in brain tissues also causes CP. Brain hypoxia and anoxia are developed as a result of cardiac abnormalities, damages to blood vessels of B, anemia, incorrect anesthesia or intoxication by chemical agents that cause methemoglobinemia. Focal
hypoxia can be a result of neoplasia, infectious or parasitic diseases. Brain hypoxia causes
brain edema. It is manifested by ataxia, tetraparesis, collapse, convulsions and coma;
mydriasis or miosis of pupils can be observed.
Feline ischemic encephalopathy syndrome may be seen as sensory-motor disorders
or seizures. The list of symptoms includes behavioral changes, tendency to aggression,
grand mal or neurological disorders that are restricted to only one side of the muzzle,
trunk or limbs. Characteristic features of ischemic encephalopathy are rapid development
and non-progressive unilateral manifestations.
Neoplasms that affect the nervous system (NS) are divided into primary, secondary
(metastatic) and skull neoplasms. Neoplasms and abscesses of B cause compression,
deformation, destruction of NT and also circulatory disorders and increase of ICP. The
first symptoms of the presence of tumors can be sporadic Ss, after which weeks or even
months pass before occurrence of the first permanent neurological symptoms.
Acta Sci. Pol.
Classification of cerebral paroxysms...
21
The most famous of viral diseases, which are accompanied by nervous symptoms, are
rabies and Aujeszky’s disease. Also canine distemper, infectious canine hepatitis, feline
infectious peritonitis and feline viral rhinotracheitis may be accompanied by nervous
manifestations.
Among neurological complications that occur in the case of canine distemper are Ss,
cerebellar lesions, balance disorders, sensory ataxia, partial paresis, myoclonus or involuntary muscular contractions, optic neuritis.
Symptoms of CNS lesions in the case of infectious canine hepatitis include oppression, disorientation, Ss and coma.
Feline infectious peritonitis is capable of causing nonsuppurative pyogranulomatous
meningitis, meningoencephalitis, ependimite. Lesion of CNS is manifested by involuntary convulsive muscle contractions, hyperesthesia.
Feline viral rhinotracheitis can cause viral encephalomyelitis. The virus has the ability
to infect the vestibular system. Neurological manifestations do not usually progress.
The phenomenon of post-vaccination encephalomyelitis was relevant in the past,
when live vaccines against rabies and combined vaccines against canine distemper and
infectious canine hepatitis were in use.
Inflammation of the brain and its membranes occupy an important place among etiological factors.
Granulomatous encephalomyelitis (granulomatous meningoencephalomyelitis) is accompanied by pyrexia, spining, blindness, convulsions, ataxia, paresis, cervical pain.
Polyencephalomyelitis of cats has various neurological manifestations, which include
behavioral abnormalities, pupillary reflex disturbances, lesions of the cerebellum, paraparesis, ataxia, symptoms of the lower motor neuron lesions.
Primary reticulosis is a progressive disease which affects mainly the forebrain. It may
be accompanied by reticulosis of eyes and granulomatous reticulitis.
Piogranulomatous meningoencephalomyelitis was described in pointers. It is clinically manifested by cervical hyperesthesia, tetraparesis, cranial nerve deficits.
Symptoms of bacterial meningitis (meningoencephalitis) include pirexia, hypersensitivity, muscular rigidity.
Clostridium tetani leads to hyperesthesia, tonic spasms of skeletal muscle with intermittent clonic convulsions.
Neurological symptoms are associated with direct invasion of the CNS in the case of
parasitic diseases, e.g. dirofilariasis, larva migrans (Toxocara larvae, Ancylostoma caninum, Angiostrongylus cantonensis), coenurosis (Taenia spp.).
Sometimes toxoplasmosis causes encephalitis and encephalomyelitis.
Most common toxins, that damage NS, cause depression, coma, tremors, ataxia, paresis, symptoms of generalized lower motor neurons lesion (Table 3) [Gwaltney-Brant et
al. 2000].
The brightly expressed spontaneous Ss often indicates poisoning. Strychnine is able
to cause tetany; chlorinated hydrocarbons – tonic-clonic seizures; organophosphates and
carbamates also cause tonic-clonic seizures and even miosis, salivation, vomiting, diarrhea and involuntary urination. Lead poisoning is usually chronic and is manifested by
depression, tremor, ataxia, symptoms of affection of GIT and Ss. Cyanides cause poliencephalomalacia.
Medicina Veterinaria 13 (1-4) 2014
22
N. Ivanczenko et al.
Table 3. Signs of intoxication
Tabela 3. Objawy zatrucia
Clinical signs of intoxication
Kliniczne oznaki zatrucia
Paroxysmal states
Stany napadowe
Inhibition/coma
Inhibicja/śpiączka
Tremor, ataxia, paresis
Drżenie, ataksja, niedowład
Possible causes of intoxication
Możliwe przyczyny zatrucia
• chlorinated hydrocarbons – węglowodory chlorowane
• organophosphates – organofosforany
• carbamates – karbamaty
• strychnine – strychnina
• sodium fluoroacetate (1080) – fluorooctan sodu
• thallium – tal
• lead (plumbum) – ołów
• staphylococcal toxin – toksyna gronkowcowa
• amphetamines – amfetaminy
• zinc phosphide – fosforek cynku
• 5-hydroxytryptophan – 5-hydroksytryptofan
• narcotic drugs – leki narkotyczne
• α-naphthyltiourea – α-naftylotiomocznik
• ethylene glycol – glikol etylenowy
• hexachlorophene – heksachlorofen
• metaldehyd – metaldehyde
• lead (plumbum) – ołów
• organophosphates – organofosforany
• chlorinated hydrocarbons – węglowodory chlorowane
• tranquilizers – środki uspokajające
Ss caused by head trauma, can have focal as well as generalized character. The damage of brain’s cortex results in Ss, abnormalities in mental status, behavioral and postural
reactivity [Lorenz and Kornegay 2004, Plat and Olby 2004, Shvarts-Porshe 2011].
Classical ischemic neuropathological changes in brain of dogs with seizures consist of
astrocytic swelling, basophilic incrustations of ischemic neurons.
Diagnostic approach
Ss occur occasionally, that is why a doctor of veterinary medicine often has to estimate
the animal’s condition without observing any of the Ss. A good idea in this case is to
encourage the owners to make video recordings of Ss in animals, that can significantly e
ease the process of diagnostics. In case of Ss, a supposition about the initial diagnosis is
primarily based on anamnesis and observation of the paroxysm.
A plan of diagnostic approach was developed to for facilitate the diagnostics. It consists of so-called “minimum database” and “complete database” (Table 4). ”Minimum
database” allows to assume the presence of the primary neurological diseases, metabolic
and systemic nervous disorders in animals. All animals which have more than one Ss
have to be examined accordingly to this plan. Animals that had only a sporadic attack
have to pass physical and neurological examination. If abnormalities were not detected,
it is still necessary to continue observation. If neurologic examination finds abnormalities, it is considered that the source of disturbance is intracranial pathology until another
diagnose is proved.
Acta Sci. Pol.
Classification of cerebral paroxysms...
23
Table 4. Database of seizure disorders
Tabela 4. Baza danych z napadów padaczkowych
Minimum Database – Minimalna baza danych
Information about the animal Species, breed, age, sex
Informacje o zwierzęciu
Gatunek, rasa, wiek, płeć
Vaccination (type of vaccine, date administered)
Szczepienie (rodzaj szczepionki, termin podania)
Living conditions, appetite, vomiting, diarrhea, sneezing/cough, polydipsia/
polyuria, body temperature
Warunki życia, apetyt, wymioty, biegunka, kichanie/kaszel, wzmożone pragnienie/poliuria, temperatura ciała
Age when the first attack occurred, its frequency and clinical course
Wiek, w którym wystąpił pierwszy atak, jego częstotliwość i przebieg kliniczny
Detailed description of CP (generalized/partial duration, aura, postictus period,
day time, dependence on physical activity, nutrition, sleep, external irritants)
Anamnesis
Szczegółowy opis PM (uogólniony/częściowy czas trwania, aura, okres poataAnamneza
kowy, pora dnia, zależność od aktywności fizycznej, odżywienia, snu, czynników drażniących zewnętrznych)
Previous and/or current illness or trauma
Poprzednia i/lub obecna choroba lub trauma
Drugs, possibility of intoxication – Leki, możliwość odurzenia
Behavioral changes, other nervous signs
Zmiany zachowania, inne objawy nerwowe
Date of copulation, accouchement
Data kopulacji, porodu
Skeletal system (parameters, skull configuration, presence of trauma
or muscle atrophy)
Układ kostny (parametry, konfiguracja czaszki, obecność urazu lub atrofii mięśni)
Physical examination
Badanie fizyczne
Cardiovascular system (mucous membranes, arrhythmias, murmurs)
Układ sercowo-naczyniowego (błony śluzowe, arytmie, szmery)
Ophthalmoscopy – Oftalmoskopia
Assessment of reflexes – Ocena odruchów
Time of the last attack, if 24–48 hours ago and the results of neurological
examination disturb, the examination should be repeated again in 24 hours for
Neurological examination
making a final conclusion
Badanie neurologiczne
Czas ostatniego ataku, jeżeli 24–48 godzin temu i wyniki badania neurologicznego niepokoją, badanie powinno być powtórzone po 24 godzinach w celu
końcowego wniosku
Making analyses and tests GBA, CBC, GUE
Wykonywanie analiz i
Toxicology tests (blood, urine, contents of IG tract)
testów
Testy toksykologiczne (krew, mocz, treść przewodu pokarmowego)
Complete Database, Kompletna baza danych
СТ / МRI, ТK/ МRI
EEG
Special types of examination Analysis of CSF (cytology, protein content, pressure)
Specjalne rodzaje badań
Analiza PMR (cytologia, zawartość białka, ciśnienie)
Radiography (projections: ventrodorsal, lateral, frontal)
Radiografia (ujęcia: brzuszno-grzbietowe, boczne, przednie)
BBA – biochemical blood analysis, EEG – electroencephalography, CBC – complete blood count, GUE – general urine examination, СТ – computed tomography, МRI – magnetic resonance imaging
BBA – biochemiczna analiza krwi, EEG – elektroencefalografia, CBC – pełna morfologia krwi, GUE – ogólne badanie moczu,
TK – tomografia komputerowa, МRI – rezonans magnetyczny
Medicina Veterinaria 13 (1-4) 2014
24
N. Ivanczenko et al.
In compiling the anamnesis it is necessary to clarify whether the Ss started with generalized and symmetric or focal signs. It is important not to confuse a period of aura with focal Ss. Any sign of focal motor activity, which precedes to generalized seizures (chewing
movements, difficulty in turning the head, clonic muscle contractions), indicates partial
Ss, even if it later becomes generalized.
CONCLUSIONS
According to the “plan-minimum” (Fig. 1), veterinarian can make supposition about the
possible cause of Ss. It is essential to establish a definitive diagnosis. Prescription of
anticonvulsants are recommended in case when Ss are cluster or occur frequently (more
than 1 per 6 weeks). “Complete database” (Fig. 1) is useful in cases when: (1) previous
examination indicate the presence of neurological disease; (2) sporadic Ss suddenly occurs in animal of geriatric age; (3) Ss can not be eliminated by drugs. If CT, MRI gives no
cues, the analysis of CSF and conduction of EEG should be done.
It should be remembered that dogs older than 5 years and cats usually have acquired
diseases. The most common reason of Ss in cats are organic diseases of B (purulent
meningoencephalitis, feline ischemic encephalopathy, tumors). In animals of geriatric
age sporadic Ss is considered a symptom of tumors until proven otherwise.
In case when any metabolic, toxic or organic causes of CP cannot be found, preliminary diagnosis “idiopathic epilepsy” is set and anticonvulsants are prescribed [Lorenz and
Kornegay 2004, Plat and Olby 2004, Shvarts-Porshe 2011].
Minimum Database – Minimalna baza danych
Sufficient data for a final diagnosis
determination, namely:
Wystarczające dane do ustalenia końcowej
diagnozy, mianowicie:
• Metabolic disorders
Zaburzenia metaboliczne
• Pathology of development
Patologia rozwoju
• Intoxication – Zatrucie
• Consequence of injury
Konsekwencja obrażeń
Elimination of the root causes.
Eliminacja źródłowych przyczyn.
Use of anticonvulsants if it is necessary.
Użycie środków przeciwdrgawkowych jeśli
konieczne.
Making the final diagnosis:
Stawianie końcowej diagnozy:
• Pathology of development
Patologia rozwoju
• Inflammatory process
Proces zapalny
• Tumors – Guzy
• Consequence of injury
Konsekwencja obrażenia
Sufficient data for preliminary
Wystarczające dane do wstępnej diagnozy
• Metabolic disorders
Zaburzenia metaboliczne
• Intoxication
Zatrucie
• Pathology of development
Patologia rozwoju
• Genetic predisposition
Predyspozycje genetyczne
• Inflammatory process
Proces zapalny
• Consequence of injuries
Complete Database
Kompletna baza danych
Data for diagnosis not sufficient
Niewystarczające dane do diagnozy
• Pathology of development
Patologia rozwoju
• Genetic predisposition
Predyspozycje genetyczne
• Inflammatory process
Proces zapalny
• Tumors – Guzy
• Consequence of injury
Konsekwencja obrażenia
Prescribing of anticonvulsants
Przepisanie leków
przeciwdrgawkowych
Therapy is not effective
Terapia jest nieefektywna
Missing data for making a diagnosis.
Brakujące dane do dokonania diagnozy.
Idiopathy is assumeg – Przyjmuje się samoistność
Repeated investigations are indicated over a period of time,
or after changes of the animal’s condition
Wskazane są badania okresowe lub po zmianie kondycji
zwierzęcia
Prescription of anticonvulsanta
Przepisanie leków
przeciwdrgawkowych
Fig. 1. Scheme of diagnosis and treatment of animals with cerebral paroxysms
Ryc. 1. Schemat diagnostyki i leczenia zwierząt z napadami mózgowymi
Acta Sci. Pol.
Classification of cerebral paroxysms...
25
REFERENCES
Berendt M., Gredal H., Alving J., 2004. Characteristics and phenomenology of epileptic partial
seizures in dogs: similarities with human seizure semiology. Epilepsy Research, 61, 167–173.
Famula T.R., Oberbauer A.M., 2000. Segregation analysis of epilepsy in the Belgian tervueren dog.
Vet Rec., 147, 218–221.
Gastant H., 1969. Clinical and electroencephalographic classification of epileptic seizures. Epilepsia, 10 (supp.), 512–513.
Gwaltney-Brant S.M., Albertsen J.C., Khan S.A., 2000. 5-Hydroxy-trytophan toxicosis in dogs: 21
cases (1989–1999). J. Am. Vet. Med. Assoc., 216, 1937–1940.
Hall S.J., Wallace M.E., 1996. Canine epilepsy: a genetic counseling programme for keeshonds.
Vet. Rec., 138, 358–360.
Holliday T.A., 1980. Seizure disorders, Ver. Clin. North Am., 10, 3–29.
Lorenz M., Kornegay J., 2004. Handbook of Veterinary Neurology. Replica Press, India, 323–342.
Oliver J.E., 1987. Seizure disorders and narcolepsy. Veterinary neurology [in:] Oliver J.E., Hoerlein
B.F., Mayhew I.G. (eds). Philadelphia, WB Saunders, 285–302.
Oliver J.E., 1980. Seizure disorders in companion animals. Compend Cont. Educ. Pract. Vet., 2,
77–86.
Oliver J.E., 1978. Protocol for diagnosis of seizure disorders in companion animals. J. Am. Vet.
Med. Assoc, 172, 824.
Plat S., Olby N., 2004. BSAVA Manual of Canine and Feline Neurology. Replica Press, India,
97–111.
Shvarts-Porshe D., 2011. Підходи до діагностики нападів у дрібних домашніх тварин.
Епілептичні і не епілептичні напади. Ветеринарна практика, 9 (59), 14–18.
KLASYFIKACJA PAROKSYZMÓW MÓZGOWYCH
U PSÓW I KOTÓW, ETIOLOGIA I DIAGNOZA
Streszczenie. Głównym celem badania było określenie prawidłowej oceny pacjenta, zrozumienie zasad terapii lekami przeciwpadaczkowymi (AED), opracowanie strategii farmakoterapii i planów leczenia w nagłych wypadkach. Dokonano przeglądu literatury klasyfikacji
stanów napadowych u zwierząt, ich czynników etiologicznych i charakterystyk przejawów.
Usystematyzowane zostały informacje na temat podstawowych zasad diagnozowania, stawiania wstępnych i końcowych diagnoz paroksyzmów mózgowych u zwierząt. Artykuł
omawia główne zasady postępowania z napadmi (napadowe zaburzenia zarządzania funkcjami mózgowymi) u psów i kotów. Szczególna uwaga poświęcona jest leczeniu padaczki
u tych gatunków.
Słowa kluczowe: klasyfikacja, diagnostyka, etiologia, napad
Zaakceptowano do druku – Accepted for print: 18.12.2015
For citation – Do cytowania: Ivanczenko N., Grom K., Pasicka E., Tsvilihovskiy M.,
2014. Classification of cerebral paroxysms in dogs and cats, their etiology and diagnosis,
Acta Sci. Pol. Med. Vet. 13 (1-4), 15–26.
Medicina Veterinaria 13 (1-4) 2014