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Abstract: The benzodiazepine withdrawal syndrome is a complex phenomenon which presents serious difficulties in definition and measurement. Drug withdrawal syndromes, in general, tend to consist of mirror images of the drugs' initial effects. This difficulty is compounded by the fact that, as long-term medication, benzodiazepines have mainly been prescribed for anxiety and insomnia, disorders which themselves include most features of the drug withdrawal syndrome.
Nevertheless, the existence of a benzodiazepine withdrawal reaction, from both high and low (therapeutic) doses of benzodiazepines, is no longer in dispute, and many attempts have been made to define and measure it and to estimate its incidence and duration.
Smith and Wesson (1983) and Ashton (1984) drew attention to the characteristic fluctuation of symptoms, which may wax and wane without obvious psychological provocation.
Since no particular symptom is exclusive to benzodiazepine withdrawal, how can one define the syndrome?
An increase in self-rated symptoms (Comprehensive Psychiatric Rating Scale) to greater than 50% of baseline levels, followed by a return to lower values.
A combination of methods (1) and (2) so that a withdrawal reaction is defined as the appearance of new symptoms that resolved before the end of the study (20 and 14 weeks after the end of withdrawal [Tyrer et al., 1983]). Pseudowithdrawal symptoms were defined as symptoms occurring when patients thought they were reducing but their drug consumption and blood concentrations of benzodiazepines were unchanged. Such definitions, derived from double-blind, placebo-controlled studies, have been extremely helpful in the recognition of benzodiazepine dependence, especially low-dose dependence. Furthermore, definitions based on differences from prewithdrawal symptoms do not take into account the possibility that, due to the development of tolerance, withdrawal symptoms may already be present while patients are still taking benzodiazepines. Because of these many immeasurable factors, it is doubtful whether the boundaries of a "true" benzodiazepine withdrawal syndrome can ever be clearly demarcated.
Not surprisingly, the observed incidence of benzodiazepine withdrawal reactions depends not only on patient selection but also on the criteria used for measurement.
The identification of the benzodiazepine withdrawal syndrome is difficult enough; its duration is even more difficult to delineate.
To a large extent the apparent duration depends upon how long the patients are followed up, and several authors have drawn attention to the prolonged nature of postwithdrawal symptoms in some cases. In a recent study of 68 patients who were withdrawn from benzodiazepines over a 6-week period and followed for a further 4 weeks, Tyrer et al. Ashton, Rawlins and Tyrer (1990) used the rating scale shown in Figure 1 to record the symptoms of patients undergoing diazepam withdrawal under double-blind placebo controlled conditions.
A further problem in assessing the duration of the withdrawal syndrome is the interpretation of the baseline (prewithdrawal) symptoms and anxiety scores. Certainly in these patients the benzodiazepines were not effectively controlling anxiety and, as argued above, it is possible that at least some of the presenting symptoms were due to "withdrawal" symptoms even in the presence of the drug, as a result of the development of drug tolerance. All the problems of definition discussed above are multiplied in any attempt to describe protracted benzodiazepine withdrawal syndromes. Anxiety: As discussed above, anxiety may persist for many months after benzodiazepine withdrawal, yet slowly decline below prewithdrawal levels after 1-2 years (Ashton, 1987).
Hence persisting anxiety after benzodiazepine withdrawal does not necessarily imply the re-emergence of an anxiety state existing before benzodiazepine treatment; it may represent the uncovering of a type of learning deficiency induced by long-term benzodiazepine use. Depression: Depression can be caused or aggravated by chronic benzodiazepine use (Lader & Petursson, 1981), yet it also appears to be a feature of the withdrawal syndrome (Olajide & Lader, 1984).
Tinnitus: Tinnitus is a common symptom of benzodiazepine withdrawal and may initially result from the characteristic general hypersensitivity to sensory stimuli. Tinnitus is fairly common in the general population and the apparent relation to benzodiazepine use may be incidental, but these cases raise the suspicion that benzodiazepines may occasionally cause permanent or only slowly reversible brain damage.
Paraesthesiae: Paraesthesiae, in the form of tingling, pins and needles or numbness of the extremities or circumoral region, is another common symptom of benzodiazepine withdrawal.
Formication is also common during benzodiazepine withdrawal, and many patients temporarily complain of a feeling of insects crawling on the skin or of lice or nits in the hair.
Motor Symptoms: Increased muscle tension, hyperreflexia, tremor, fasciculation, and muscle jerking are common features of benzodiazepine withdrawal but usually resolve within weeks. Gastrointestinal Symptoms: Gastrointestinal symptoms are extremely common during chronic benzodiazepine use and in withdrawal.
The primary effect of benzodiazepines is enhancement of gamma-aminobutyric acid (GABA) activity on postsynaptic GABA-A receptors in the brain. Any chronically used drug gradually engenders a series of homeostatic responses which tend to restore normal function despite the presence of the drug. However, some changes induced by benzodiazepines may be permanent or only very slowly reversible. Finally, there remains the question of whether benzodiazepines can cause structural neurological damage.
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Thus, abrupt withdrawal from chronic usage of beta adrenoceptor antagonists such as propranolol may give rise to tachycardia and palpitations; abrupt withdrawal from antihypertensive doses of clonidine may be followed by hypertension, anxiety, and other signs of increased sympathetic activity. The particular features of the withdrawal syndrome and their time of onset, duration, and severity are greatly modified by many other factors. When such patients undergo reduction of benzodiazepine dosage, especially slow reduction, how can one specify which emergent symptoms are "true", drug-related withdrawal symptoms, which are "pseudowithdrawal" symptoms (Tyrer, Owen, & Dawling, 1983), which represent a return of the original anxiety state, and which are the natural reactions of an anxious personality undergoing the stress of withdrawal? Smith and Wesson (1983) suggest that this wavelike symptomatology is an important marker for distinguishing the low-dose benzodiazepine withdrawal syndrome from symptom re-emergence. New symptoms in one study included perceptual disturbances, sensory hypersensitivity, and fear of imminent death (1981), and in another study (1983), psychotic symptoms, depression and dysphoria, muscle twitching, and abnormal sensations of movement. Symptom resolution is clearly an important feature in differentiating between symptoms due to withdrawal and symptom re-emergence, emergence, or overinterpretation. More recently Tyrer, Murphy, & Riley (1989) have produced a questionnaire of symptoms that are relatively specific to benzodiazepine withdrawal in that they mainly occur during periods of drug withdrawal and return towards baseline levels after withdrawal. However, they are of necessity arbitrary and can only be approximate, since the appearance or severity of any particular symptom or symptom cluster may actually represent a variable combination of true withdrawal, pseudowithdrawal, and re-emergence of anxiety, and the same patients liable to pseudowithdrawal reactions are also likely to be most vulnerable to true withdrawal effects.
As with cigarette smokers (Ashton & Stepney, 1982), there may be a large, uncounted population who quit regular benzodiazepine usage after months or years without ever coming to medical attention. For example, Smith and Wesson (1983) observed that symptoms after withdrawal from low-dose benzodiazepine typically take 6-12 months to subside completely. Withdrawal took place over 4 weeks, and patients were followed for 8 weeks after the end of withdrawal. Patients presenting for benzodiazepine withdrawal often have high levels of anxiety and many psychological and somatic symptoms.
Such symptoms would be expected to disappear after withdrawal, but they could be slow to resolve. Is it possible to pinpoint a time at which the benzodiazepine withdrawal syndrome ends and to say with certainty that any residual symptoms must be due to other factors? Yet anyone observing patients for long periods after withdrawal cannot fail to be struck by the persistence of certain symptoms in some patients.
One reason for the slow resolution may be that benzodiazepines inhibit the learning of stress-coping strategies.
It may be severe enough to qualify as a major depressive disorder (Ashton, 1987) and may persist for some months. Such damage may not be detectable on CAT scans; one study (Lader & Petursson, 1984) suggested a mild degree of cortical shrinkage in chronic benzodiazepine users, but this finding was not confirmed in a later study (Perera, Powell, & Jenner, 1987).
Occasionally, more bizarre sensations are reported, such as a feeling of slime or water running over the body, a sense of inner vibration, or a feeling of "trembling inside", and these symptoms may be protracted. Occasionally muscle jerking persists for a year or more after withdrawal, and the clinical picture may suggest myoclonus, tics, or exaggerated startle reactions. Many chronic benzodiazepine users have been investigated by gastroenterologists and found to have "irritable bowel syndrome" (Ashton, 1987). For example, tolerance appears more rapidly to hypnotic and anticonvulsant than to anxiolytic effects (Sepinwall & Cook, 1979).

Cessation of the drug exposes all the adaptations which have accrued to counteract its presence, releasing a rebound of unopposed activity involving many neurotransmitters and their receptors and many brain systems.
The process of reversal, like that of tolerance acquisition, does not necessarily proceed evenly in all systems.
Since benzodiazepines apparently inhibit learning, especially for coping with stress strategies (Gray, 1987), cessation after many years of use may expose a learning deficit, especially in the ability to cope with stress. Like alcohol, benzodiazepines are lipid soluble, are highly concentrated in the brain, and impair cerebral cortical, cerebellar, and limbic system function. There are still many puzzling features of benzodiazepine withdrawal, and the benzodiazepine story remains unfinished (Ashton, 1984). Scores for selected symptoms before, during, and after diazepam withdrawal(n = 11; mean total scores on withdrawal symptoms scale shown in Figure 1. If you reside in an EU member state besides UK, import VAT on this purchase is not recoverable. Many withdrawal symptoms are a result of pharmacodynamic tolerance to benzodiazepines, some mechanisms for which are discussed. Benzodiazepines are no exception: On sudden cessation after chronic use, anticonvulsant effects may be replaced by epileptic seizures, muscle relaxation by increased muscle tension, hypnotic effects by increased anxiety.
Such factors include pharmacokinetic variables, dosage and duration of drug use, rate of withdrawal, the presence or absence of the original disorder (such as anxiety) for which the drug was prescribed, personality characteristics, physical makeup and susceptibility, and the use of concomitant treatments. In circumstances such as these, the benzodiazepine withdrawal syndrome becomes largely a matter of definition. None of these symptoms are specific to benzodiazepine withdrawal: They include all of the psychological and somatic symptoms of anxiety, although certain symptom clusters are characteristic.
However, since symptoms may fluctuate in the course of the day or over periods of days or weeks, accurate recording is difficult. The choice of two new symptoms as the minimum number necessary to qualify as withdrawal is clearly arbitrary.
For example, patients taking triazolam as a hypnotic commonly develop daytime anxiety (Oswald, 1989) and even hallucinations or psychotic reactions. Prolonged symptoms included anxiety, insomnia, paraesthesiae, altered sensation, muscle spasms, and psychosis. Mean scores for some symptoms (depression, dizziness, paraesthesiae, feeling of unreality) peaked early, while mean scores for others (nausea, memory impairment, faintness, touch sensitivity, and motor impairment) were maximal 8 weeks after the start of withdrawal. Figures 2 and 3 show Hospital Anxiety Depression (anxiety) (Zigmond & Snaith, 1983) and symptom rating scores for 12 patients on benzodiazepines compared with the scores of 18 healthy university students approaching their exams.
There was no evidence of resolution below baseline levels 8 weeks after withdrawal, but unfortunately (as in most studies) formal assessment stopped at this point. The problem is similar to that of designating which effects of a bout of influenza or infectious mononucleosis can be attributed to the specific virus. These may not be "true" benzodiazepine withdrawal symptoms; nevertheless they are possibly related to benzodiazepine use and often present a clinical problem. Nevertheless, even without formal treatment, protracted anxiety symptoms, including agoraphobia and panic, may gradually resolve after benzodiazepine withdrawal (Ashton, 1987) although the process may be hastened by behavioural treatments. Olajide and Lader (1984) suggest that the mechanisms for postwithdrawal depression may be central serotonin depletion, but there is no direct evidence for this.
First noticed tinnitus, mainly right-sided, on withdrawal from flurazepam 30mg daily in 1985. Benzodiazepines depress the sensitivity of the respiratory centre to carbon dioxide (Gilmartin, Corris, Stone, Veale, & Gibson, 1988) and it is possible that the respiratory centre becomes hypersensitive during withdrawal, triggering hyperventilation. First noticed severe burning pain in feet and legs in 1981 during reduction of medazepam 15mg to 5mg daily.
Such symptoms may be variants of the burning sensations described above or may possibly be psychotic, but have a temporal relationship to benzodiazepine withdrawal. Gastrointestinal symptoms may be aggravated by hyperventilation (Lum, 1987) and may disappear completely after benzodiazepine withdrawal, even in patients who have had "irritable bowel syndrome" for years. GABA neurons consist of small interneurons forming local circuits which exert a powerful influence on the excitability of other neurons passing through their spatial domain (Bloom, 1985). Such changes consist of decreased sensitivity of these receptors to GABA, probably as a result of alterations in affinity state and decreased density (Cowan & Nutt, 1982; Nutt, 1986). Tolerance to different effects may also vary between individuals, possibly due to variations in intrinsic GABA activity in different parts of the brain, which are in turn reflected in personality characteristics and susceptibility to stress.
Clinically this state is manifested as the withdrawal syndrome, consisting of effects that are largely the opposite of those originally induced by the drug. The variable time of emergence and duration of individual symptoms during benzodiazepine withdrawal noted by Tyrer (1989) and Ashton et al.
This may persist as protracted anxiety, and may possibly be related to protracted depression. It is possible that use over many years could cause physical changes such as cortical shrinkage, which may be only partially reversible.
Tolerance to and physical dependence on alcohol: Behavioural and neurobiological mechanisms. Abstinence symptoms after withdrawal from tranquillising drugs: Is there a common neurochemical mechanism? Depression following withdrawal from long-term benzodiazepine use: A report of four cases. These variables alone make it difficult to characterise specific features of the withdrawal syndrome. Owen and Tyrer (1983) and Petursson and Lader (1981a & b) emphasised the appearance of new symptoms, not experienced before withdrawal and uncommon in anxiety states. 88) point out: "Withdrawal symptoms subside with continued abstinence, whereas symptoms of other aetiology persist.
These are almost certainly withdrawal effects since they are immediately relieved by taking the drug but eventually disappear after the drug is stopped (Ashton, 1987). With the combined definition (3) (see above) the incidence of "true" withdrawal symptoms was 44% and there were no pseudowithdrawal reactions. Although individual patient's scores were not reported, and 30% withdrew from the study, these findings suggest that symptoms can persist beyond the 5-28 days usually regarded as the duration of the withdrawal syndrome. Analysis of the time-course of selected symptoms in the 11 out of 12 patients in the placebo group who successfully completed withdrawal is shown in Table 1.
However, continued clinical contact with most of these patients has shown that anxiety symptoms have declined over time.
Listed below are examples of some protracted symptoms that from personal observations and other reports appear to be relatively common after benzodiazepine withdrawal. Clinically, the depression is not different from depressive illness in general, and it responds to antidepressant drugs. Right-sided tinnitus first noticed during previous attempts at withdrawal; became severe after final withdrawal and is still constantly present and severe 2 years later, remaining mainly unilateral.
Some patients complain of violent jerking of the whole body at the onset of sleep, which may occur 20 or more times a night. Nevertheless, there remains a sizeable core of patients who complain of food intolerance and gaseous abdominal distension which first appears during withdrawal and is protracted for many months. Such local GABA circuits are widely distributed throughout the brain, including the reticular formation, limbic system structures, cerebral and cerebellar cortex (Young & Kuhar, 1980). Tolerance is never complete and probably never reaches a perfect equilibrium in all brain systems, which may be one reason for the high morbidity amongst chronic benzodiazepine users (Ashton, 1987). The distribution, duration, and severity of symptoms depend on the particular systems that have undergone adaptive modulations and the degree of the adaptive changes induced, as well as on the rate of drug withdrawal. Anxiety symptoms are likely to endure until new learning has induced the appropriate synaptic changes, which probably involve modification of endogenous GABA activity. A double blind placebo controlled study of buspirone in diazepam withdrawal in chronic benzodiazepine users.
Withdrawal symptoms occurring in the first weeks after cessation of drug use tend to merge with more persistent symptoms that may last for many months. Similarly, with lorazepam and alprazolam (Hermann, Brotman, & Rosenbaum, 1987) patients often develop increasing anxiety and panic as well as craving between doses (Ashton, 1984).
It is also worth noting that withdrawal syndromes in the form of rebound insomnia (Kales, Scharf, & Kales, 1978) or more general symptoms can occur in experimental subjects and in nonanxious patients prescribed benzodiazepines for sports injuries (Lader, 1988).

This incidence of course only applies to those consenting to take part in the study and managing to finish it. Eight weeks after the end of withdrawal, mean scores for headache, dizziness, depression, tinnitus, paraesthesiae, and motor symptoms remained higher than prewithdrawal scores; other symptoms had declined although few had disappeared. Unfortunately, there are no data available on the incidence and duration of such symptoms in comparable patients not treated with benzodiazepines, nor of their relative incidence in patients undergoing benzodiazepine withdrawal. Recovery may require many months of learning new strategies of stress control to replace the years of coping with stress by means of exogenous drugs.
It is not clear whether protracted depressive symptoms are more common in patients with a previous history of depression or whether it recurs in subsequent years after withdrawal. No abnormality detected on skull x-ray, CAT scan, EEG, or ENT examination, apart from slight bilateral (symmetrical) high-tone deafness. Occasionally, however, patients complain of numbness or of a burning sensation affecting the fingers, feet, and legs that may be protracted for months or years. Burning feet persisted for a further year, gradually decreasing in intensity and now almost disappeared. Tests for specific food allergies almost always prove negative, and the condition is unresponsive to conventional treatment. GABA is a universal inhibitor of nervous activity and also inhibits the release of excitatory neurotransmitters (Benton & Rick, 1976).
The whole complex of primary and secondary changes eventually results in benzodiazepine tolerance.
Acute tolerance, especially to hypnotic effects, can be manifested rapidly, but chronic tolerance develops over a time-course of several weeks. Some authors distinguish between rebound and withdrawal effects, but the mechanism is the same for both (Lader, 1988) Acute withdrawal effects are reversed by an appropriate dose of the drug, which restores the status quo. The perturbations of brain function induced by benzodiazepines are exceedingly complex, and it is not surprising that withdrawal symptoms are many and variable. These prolonged symptoms do not necessarily constitute "true" pharmacological withdrawal symptoms, but are nevertheless related to long-term benzodiazepine use. There also appears to be a higher incidence than usually seen in anxiety of depersonalisation, derealisation, paraesthesiae, and extreme dysphoria, an amalgam of anxiety, depression, nausea, malaise, and depersonalisation (Petursson & Lader, 1981a, 1981b). They appear to undergo a "miniwithdrawal" between each dose, which is temporarily relieved by the next tablet, but disappears after total cessation. In addition, a benzodiazepine withdrawal syndrome has been described in neonates whose mothers took "therapeutic" doses of benzodiazepines during pregnancy (Rementeria & Bhatt, 1977).
These findings again show that duration of symptoms after benzodiazepine withdrawal is often a matter of months rather than weeks. It is clear that the patients had considerably higher scores than the normal subjects on both scales, even at the beginning of the study while they were still taking benzodiazepines.
Do they include the period of postviral lethargy and depression which, like benzodiazepine withdrawal symptoms, tends to recur in wave-like fashion for several months?
Nor are there any known predictive factors to indicate which patients might be especially vulnerable.
Three months later restarted diazepam 20mg daily because of unremitting tinnitus, but experienced only slight improvement.
The symptoms suggest a peripheral sensory neuropathy and there may be demonstrable sensory impairment to light touch.
Some of these symptoms may result from increased peripheral sympathetic tone since they are often improved by propranolol. Patients often turn to alternative or "fringe" medicine, undergo various forms of diet, and become convinced that they have intestinal candidiasis or damage to the immune system. Thus the actions of benzodiazepines include not only enhancement of GABA activity at many brain sites but also decreased release of acetylcholine, noradrenaline, dopamine and serotonin (Faefely, Pieri, Pole, & Schaffer, 1981). Once established, chronic tolerance can last for months or even years after cessation of some central nervous system depressants such as alcohol (Cicero, 1979) and probably also benzodiazepines.
Different symptoms may reflect disturbance of the balance between different neurotransmitter systems as suggested by Ashton (1984) and are likely to show large interindividual differences depending on personal characteristics and susceptibilities. Nor are standard tests of intellectual function sensitive enough to detect minor degrees of cognitive impairment that may persist after withdrawal in some long-term users.
Such symptoms can include anxiety, which may partly result from a learning deficit imposed by the drugs, and a variety of sensory and motor neurological symptoms. Visual hallucinations, distortion of body image, psychotic reactions, formication, muscle fasciculation and twitching (occasionally resembling myoclonus), and considerable loss of weight are also described during benzodiazepine withdrawal and are unusual in anxiety states.
An analagous condition is seen with alcohol: alcoholics commonly complain of tremor and insomnia, symptoms which are temporarily relieved by alcohol but which only disappear after a period of abstinence. Thus the incidence of benzodiazepine withdrawal, like its diagnosis, becomes largely a matter of definition. Once again, the benzodiazepine withdrawal syndrome appears to slip through the fingers and one is led back to a question of definition. Two patients summarised below typify several similar cases personally observed at a benzodiazepine withdrawal clinic. Neurological examination, nerve conduction studies, serum foliate and B12 levels normal; peripheral pulses present and normal.
None of these claims have scientific support, although Lum (1987) reports that hyperventilation provokes histamine release and that the incidence of food intolerance and pseudo-allergic reactions is high in chronic hyperventilators. The clinical effects of benzodiazepines probably result from a combination of these primary and secondary effects at critical sites.
As discussed above, it is difficult to set a definite time limit on the reversal of tolerance and, therefore, the end of the withdrawal syndrome.
It remains possible that some protracted benzodiazepine withdrawal symptoms (including tinnitus and other neurological and psychological symptoms) could result from physicochemical neuronal damage. The protracted nature of some of these symptoms raises the possibility that benzodiazepines can give rise not only to slowly reversible functional changes in the central nervous system, but may also occasionally cause structural neuronal damage. Even with long-acting benzodiazepines such as diazepam, there is usually a history in long-term users of steadily increasing anxiety, with the development over the years of new symptoms such as agoraphobia, often with perceptual distortions and depersonalisation, despite continued usage of these supposedly anxiolytic drugs. Olajide and Lader (1984) suggested that depression may be an integral part of the benzodiazepine withdrawal syndrome and may last several months after withdrawal in susceptible individuals; this phenomenon was also observed by Ashton (1987). Probably a clear definition of duration is impossible because drug-induced perturbations of central neurotransmission merge imperceptibly into the background of individual, genetically determined, and learned patterns of brain activity. Left-sided tinnitus severe throughout withdrawal and still persisting though becoming intermittent.
Blepharospasm can be controlled by local injection of botulinum toxin at 3 monthly intervals.
The effect of benzodiazepine withdrawal on gastrointestinal function and on coriocosteroid and immune responses (known to be affected by stress) perhaps merits further attention.
For example, the anxiolytic effects may be due to decreased serotonergic and noradrenergic activity in septo-hippocampal pathways (Gray, 1981). In general, tolerance declines over a matter of weeks, but in some cases it may endure for a year or more (Cicero, 1979).
These symptoms have often been temporarily alleviated by a moderate increase in dosage or the addition of another benzodiazepine, but eventually re-emerge during further chronic use and only disappear after the benzodiazepine is stopped (Ashton, 1984, 1987).
Busto, Fornazzari, and Naranjo (1988) described two cases in whom severe tinnitus first appeared during benzodiazepine withdrawal and persisted for 6 and 12 months after discontinuation before finally diminishing or disappearing. Protracted motor symptoms such as these raise the possibility that benzodiazepines are capable of causing long-term hyperexcitability of motoneurons or central motor pathways. Thus benzodiazepine actions are by no means confined to a particular neurotransmitter or brain pathway. Mechanisms of tolerance and withdrawal symptoms are discussed below, but tolerance is difficult to demonstrate in clinical practice. In one of these cases the tinnitus was immediately alleviated by diazepam in a double-blind placebo-controlled trial conducted over 1 week, 6 months after withdrawal; after a further 6 months of abstinence the tinnitus had became tolerable.

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